Bone Anatomy


Bone Anatomy

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Introduction:

There are lots of clinical symptoms in elderly patient’s. Among these problems, low back pain is one of the most common and agonizing symptoms, some times that becomes a chronic one. Back pain is considered chronic when there is no relief after months of pain, which requires an accurate diagnosis to determine the treatment that is most likely to help.1

The skeleton is not only an adaptable and well articulated frame, but also a dynamic mineral reserve bank in which the body stores its calcium and phosphorus in a metabolically stable and structurally useful way. In 1993 experts of osteoporosis consensus development conference in Hong Kong define osteoporosis as a metabolic disease characterized by low bone mass and micro architectural deterioration of bone tissue leading to enhanced bone fragility and consequent increase in fracture risk.2 The World Health Organization (WHO) defines osteoporosis as a bone density more than 2.5 standard deviation (SDs) below the young adult mean value (T-score < – 2.5). Values between 1 & 2.5 SDs below the young adult mean are termed “osteopenia”.3

In normal individuals bone mass increases during skeletal growth to reach a peak between the ages of 20 and 25 but fall there after in both sexes.4 Increased sex hormone production at puberty is required for skeletal maturation, which reaches maximum mass and density in early adulthood. Nutrition and life style also play an important role in growth, though genetic factors are the major determinants of peak skeletal mass and density. Peak bone mass is often lower among individuals with a family history of osteoporosis. After the age of 30 to 45, however the resorption and formation process become imbalanced, and resorption exceeds formation.5

Aging is a natural process. Osteoporosis is a major age related disease. Menopause is associated with decline in ovarian production of estrogen. Trabecular or cortical bone loss accelerates in women after natural menopause.

In most cases, osteoporosis remaining a silent disease, until a fracture of femur or lumber vertebra occurs. Its mains clinical significance lies in the predisposition to fracture, particularly of the wrist, vertebra, and proximal femur. It is well known that the development of one osteoporotic fracture markedly increases the relative risk of a second fracture as much as 20 folds.7

As the risk of fracture increases exponentially with age, changing population demographics will increase the burden of disease (currently costing almost 1 billion pound annually in the U.K.). The lifetime risk of hip fracture for white women at age 50 is around 15%, 5% for men, with equal risk around 11-13% for colles’ or vertebral fracture. Of those surviving to 80 years of age, 30% of women and 15% of men will suffer hip fracture.3

Bone strength is closely correlated with bone mineral density (BMD). In recent years, Prospective study have been shown that BMD can predict fracture risk more early than any other conventional investigating modalities.8 It is not possible to learn how strong or weak ones bone are from a blood test or a risk factor quantification. The only way to determine osteoporotic changes in the skeleton is to measure bone density directly, for which Dual energy X-ray absorptiometry (DEXA) bone mineral densitometry is very much useful non-invasive method.9

The prevalence of osteoporosis seems daunting, and the consequences, especially in elderly peoples, appear inevitable, it is still not a high enough health care priority in developing countries like Bangladesh.

The present study was conducted among the elderly patient’s admitted with low back pain to evaluate the frequency of osteoporotic changes in skeleton, and the associated risk factors which could have bearings in prevention and reduction of morbidity & mortality of osteoporosis in Bangladesh.

 

 

 

BONE ANATOMY AND PHYSIOLOGY  

 

Normal skeletal system:

The skeletal system is a vital to life as any organ system because it plays an essential role in mineral homeostasis, houses hematopoietic elements, provides mechanical support for movement, and protects and determines the attributes of body size and shape. The skeletal system is composed of 206 bones that vary in size and shape (trabecular, flat, cuboid), and this diversity is an example of how form reflects function. The bones are interconnected by a variety of joints that allow for a wide range of movement while maintaining stability. 10

 

Bone embryology-

The skeletal system develops from mesenchyme, which is derived from the mesodermal germ layer and from neural crest. Some bones, such as the flat bones of the skull, undergo membranous ossification: that is mesenchyme cells are directly transformed in to osteoblast. In most bones, such as the long bones of the limbs, mesenchyme condenses and form hyaline cartilage models of bones. Ossification centers appear in these cartilage models, and bone gradually ossifies by endochondrial ossification.

The skull consists of the neurocranium and viscero cranium (face). The neurocranium includes a membranaous portion, which forms the cranial vault, and cartilaginous portion (chondrocranium), which form the base of the skull. Neural crest cell from the face, most of the cranial vault, and prechordal part of the chondrocranium (the part that lies rostal to the notochord). Paraxial mesoderm form the remainder of the skull.

Limbs form as buds, along the body wall that appear in the fourth weak Lateral plate mesoderm forms the bones and connective tissue, while muscle cell migrate to the limbs from the somites of the AER regulates limbs out growth and ZPA controls antero posterior patterning.

The vertebral column and ribs develop from the sclerotome compartment of the somites, and the sternum is derived form mesoderm in the ventral body wall. A definitive vertibra is formed by condensation of the caudal half of one sclerotome and fusion with the cranial half of the subjacent sclerotome.11

In endochondral ossification , in which an initial cartilage template is invaded by vascular tissue containing osteoprogenitor cells. The cartilage in them replaced by bone that extends from the centers of ossification situated in the middle and ends of the developing bone. A thin remnant of cartilage remains at each end of the bone during child hood, and is referred to as the growth plate or epiphysis. Growth depends on division of chondrocytes with in the epiphysis. Cell division takes place in the proliferative zone nearest the end of the long bone, and newly formed chondrocytes migrate downwards and enlarge in the hypertropic zone, chondrocyte death ensues and surrounding matrix calcifies before being removed and replaced by mature bone. During puberty, the rise in circulating levels of sex hormones halts cell division in growth plate. The cartilage remnant then disappears as the epiphysis fuse, and longitudinal bone growth ceases. 4

Bone Anatomy & Histology-

Bone is a type of vascularized dense connective tissue with cell embedded in a matrix composed of organic material, mainly collagen fibers, and inorganic salt rich in calcium & phosphate.12

Types of bone-

Gross observation of bone in cross section shows dense areas without cavity-corresponding to compact bone and areas with numerous interconnecting cavities corresponding to cancellous (spongy) bone. Under microscope, however both compact bone and trabeculae separating the cavites of cancellous bone have the same basic histologic structure.

In long bone, the bulbous end called epiphysis, are composed of spongy bone covered by a thin layer of compact bone. The cylindrical part- diaphysis is almost totally composed of compact bone, with a small component of spongy bone on its inner surface around the bone marrow cavity. Short bones usually have a core of spongy bone completely surrounded by compact bone. The flat bone that form the calvaria have two layers of compact bone called plates (table), separated by layer of spongy bone called the diploe. 13  Cortical bone constitute roughly 80% of the adult skeleton and predominates in the shaft of the long bone. 14

Microscopic examination of bone shows two varieties: primary, immature, or woven bone and secondary, mature or lamellar bone. Primary bone is the first bone tissue to appear in embryonic development and in fracture repair and other repair processed, it is characterized by random deposition of tissue collagen fibers, in contrast to the organized lamellar deposition of collagen in secondary bone.

Primary bone tissue –

Primary bone tissue is usually temporary and is replaced in adults by secondary bone tissue except in a very few places in the body. e.g. near the suture of the flat bones of the skull, in tooth sockets and in the insersion of some tendons.

Secondary bone tissue –

Secondary bone tissue is the variety usually found in adult. It characteristically shows collagen fibers arranged in lamellae. The whole complex of concentric lamellae of bone surroundings a canal containing blood vessels, nerves and loose connective tissue is called Haversian system or osteon. In compact bone lamellae exhibit outer circumferential lamellae.

Each Haversian system is a long, often bifurcated cylinder parallel to the long axis of the disphysis. It consists of a central canal surrounded by 4-22 concentric lamellae. The Haversian canals communicate with the marrow cavity, the periosteum and one another through transverse or oblique Volkmann’s canal. Volkmann’s canals do not have concentric lamellae; instead, they perforate the lamellae. 13

Bone marrow-

The medullary cavity in long bones and the interstices of cancellous bone are filled with red or yellow marrow. At birth all the marrow of all the bones is red, active haemopoiesis is going on every where. As age advanced the red marrow atrophies and is replaced by yellow, fatty marrow with no power of haemopoiesis. This change begins in the distal parts of the limbs and gradually progresses proximally. By young adult life there is little red marrow remaining in the limb bones, and that only in their cancellous ends; ribs, sternum, vertebrae and skull bones contain red marrow throughout life.12

Periosteum & endosteum-

 

The outer surface of the bones is covered with a thick layer of vascular fibrous tissue. This layer is the periosteum and nutrition of the underlying bone substance depends on the integrity of its blood vessels. The periosteum is osteogenic, its deeper cell differentiating into osteoblast when required. In the growing individual new bone is laid down under the periosteum, and even after growth has ceased the periosteum retains the power to produce new bone when it is needed. eg. in the repair of fracture. The periosteum is united to the underlying bone by collagen (Sharpey’s) fibers, particularly strongly over the attachment of the tendon and ligaments. Periosteum does not, of course, cover the articulating surface of the bones in synovial joints, it is reflected from the articular margins to join the capsule of the joint. The single layered endosteum that lines inner bone surface (marrow cavity and vascular canals) is also osteogenic and contributes to new bone formation.4

Composition of bone –

Cellular component – bone is composed of cellular and non cellular components. The three most specialized cell types necessary for metabolic activities of bone are osteoblasts, osteoclasts and osteocytes. 14

Osteoblasts – are derived from pleuripotential bone marrow stem cells that are capable of differentiation into fibroblastic, adipocytic, or chondrocytic / osteoblastic lineages. A critical signal for osteoblastic differentiation is provided by expression of the transcription factor cbfa-1. When dormant osteoblasts  ( bone-lining cell) on the bone surface are activated to mature osteoblasts, they synthesize uncalcified bone matrix, or osteoid, and then  promote its subsequent mineralization. Osteoblasts express specific receptor  for parathyroid hormone (PTH), 1, 25 – dihydroxy vitamin D (1,25 [OH]2 D), insulin like growth factor 1, insulin, interleukin-1, interleukin-6, interleukin-11, thyroid hormone, estrogen, androgen, and glucocorticoids.14 Some osteoblasts  are gradually surrounded by newly formed matrix and become osteocyte. During this process a space called lacuna is formed. Lacunae are occupied by osteocytes and their extension. 13

Osteocytes – Osteocytes which derive from osteoblasts, lie in the lacunae situated between lamellae of matrix. Only one osteocyte is found in each lacuna.5  They communicate with each other and surface cells via an intricate network of tunnels through the matrix known as canaliculi. The osteocytic cell processes traverse the canaliculi, and their contracts along gap junctions allow the transfer of surface membrane potentials and substrates. The large number of osteocytic processes and their distribution through out bone tissue enable them to be the prime cell in several biological processes. Osteocytes  also have the capability to detect mechanical forces and translate them in to biologic activity, including the release of chemical mediators by signal transduction pathways involving cyclic adenosine monophosphate.15

Osteoclasts – The osteoclast is the cell responsible for bone resorption is derived from haematopoietic progenitor cell that also give rise to monocytes and macrophages. Cytokines crucial for osteoclast differentiation and maturation include interleukin (IL)-1, IL-3, IL-6, IL-11, tumor necrosis factor (TNF), granulocyte – macrophage colony stimulation factor (GM-CSF), and macrophage colony stimulating factor (M-CSF).16  Osteoclasts and their progenitors appear to lack receptor for PTH, various cytokines, vitamin D, and other hormones that regulate osteoclastogenesis.17 Osteoclast are very large, branched motile cells.  Dilated portion of the cell body contain from 5 to 50 (or more) nuclei. In areas of bone undergoing resorption, osteoclasts lie within Howship’s lacunae. In active osteoclasts, the surface facing bone matrix is folded in to irregular often subdivided projections, forming a ruffled border. Surrounding the ruffled border is a cytoplasmic zone –  the clear zone that is devoid of organelles, yet rich in actin microfilaments. This zone is a site of adhesion of osteoclast to the bone matrix and creates a micro environment in which bone resorption occurs. The osteoclast secretes collagenase and other enzymes and pumps protons in to a sub cellular pocket, promoting the localized digestion of collagen and dissolving calcium salt crystals. 18

Non cellular components :- The non cellular components of bone include the organic matrix and inorganic matrix, which comprise roughly one third and two third respectively of total bone mass.14  The organic matter is mainly protein.19 Type -1  collagen, the most abundant structural protein in bone, make up 90% of the organic matrix. Other proteins in bone include small amounts of other collagens and a host of non collagenous proteins, including osteonectin, osteocalcin, osteopontin, fibronectin, thrombospondin, bone sialo protein, proteoglycans, and serum protein.20 The non collagenous protein of bone are bound to the matrix and grouped according to their functions as adhesion protein, calcium binding proteins, mineralization proteins, enzymes, cytokines, and growth factors.21 Of these only osteocalcin is unique to bone. It is measurable in the serum and used as a sensitive and specific marker for osteoblast activity.22 Osteonectin, a bone specific protein linking mineral to collagen.23   Inorganic matter represent about 50% of the dry weight of bone matrix. Calcium and phosphorus are especially abundant, but bicarbonate, citrate, magnesium, potassium, and sodium are also found. Calcium and phosphorus form hydroxyapatite crystals with the composition Ca10 (PO4)6(OH)2. Significant quantities of amorphous (non crystalline) calcium phosphate are also present. In electron micrographs, hydroxyapatite crystals of bone appear as pales that lie along side the collagen fibrils but are surrounded by ground substance. The surface ions of hydroxyapatite are hydrated, and a layer of water and ions forms around the crystal. This layer , the hydration shell, facilitates the exchange of ions between the crystal and the body fluid.24

Bone modeling and remodeling: – Osteoblasts and osteoclasts act in coordination and are considered the functional unit of bone known as the basic multicellular unit. The process of bone formation and resorption are tightly coupled, and their balance determine skeletal mass at any point in time.16  Throughout the life, bone is being constantly reabsorbed and new bone is being formed. The calcium in bone turns over at a rate of 100% per year in infants and 18% per year in adults. About 5% of bone mass is being remodeled in human skeleton at any one time. The renewal rate for bone is about 4% per year for compact bone and 20% per year for trabecular bone.25 In the formation and maintenance of skeletal system, osteoblast provides much of the local control because it not only produce bone matrix, but also plays an important role in mediating osteoclast activity. Many of the primary stimulators of the bone resorption, such as parathyroid hormone, parathyroid hormone- related protein (PHRP), IL-1 and TNF have minimal or no direct effect on osteoclast. The osteoblast has receptors for these substances, and evidence suggests that once the osteoblast receives the appropriate signals it release a soluble mediator that induces osteoclast bone resorption. The cytokine and growth factor, especially TGF-β, released from the matrix during its digestion act as a feedback loop and trigger the formation and activation of osteoblast to synthesize and deposit an equivalent amount of new bone in the resorption pit1. Osteoclast mediated resorption of bone takes place in scalloped spaces ( Howship’s lacunae) where the osteoclasts are attached through a specific αv β3 integrin to components of the bone matrix such as osteopontin. The osteoclast form a tight seal to the underlining matrix and secrets protons, chloride, and proteinases in to a confined space linked to an extra cellular lysosome. The active osteoclast surface forms a ruffled border that contains a specialized proton-pump ATPase, which secretes acid and solubilizes the mineral phase. Carbonic anhydrase with in the osteoclast generates the needed protons. The bone matrix is reabsorbed in the acid environment adjacent to the ruffled border by proteases that act as low PH,  such as cathepsin-k.

New bone, whether formed in infants or in adult during repair, has relatively high ratio of cell to matrix and is characterized by coarse fiber bundle of collagen that are interlaced and randomly dispersed (woven bone). In adult, the more mature bone is organized with fiber bundles regularly arranged in parallel or concentric sheets (lamellar bone). In long bones, deposition of lamellar bone in a concentric arrangement around blood vessels forms the Haversian system. The growth in length of bones is dependent on proliferation of cartilage cells and on the endochondrial sequence at the growth plate. Growth in width and thickness is accomplished by formation of bone at the periosteal surface and by resorption at the endosteal surface, with the rate of formation exceeding that of resorption. In adult, after the growth plate close, growth in length and endochondral bone formation cease, except for some activity in the cartilage cells beneath the articular surface.

Remodeling of bone occurs along lines of force generated by mechanical stress. This signal from these mechanical stresses is sensed by osteocytes, which transmit signals to osteoclasts or osteoblast or their precursors. A bowing deformity increase new bone formation at concave surface and resorption at convex surface, seemingly designed to produce the strongest mechanical structure. Bone plasticity reflects the interaction of cells with each other and with the environment. The product of osteoblast and osteoclast activity can assist in the diagnosis and management of bone disease. Osteoblast activity can be assessed by measuring serum bone specific alkaline phosphatase.  Similarly, osteocalcin, a protein secreted from osteoblast, is made virtually only by osteoblast. Osteoclast, activity can be assessed by measurement of products of collagen degradation.

The cycle of bone remodeling is carried out by the basic multicellular unit (BMU), comprising a group of osteoclasts and osteoblasts. In cortical bone , the BMUs tunnel through the tissue, where as in cancellous bone, they move across the trabecular surface. The process of bone remodeling is initiated by contraction of the lining cell and recruitment of osteoclast precursors. These precursors fuse to form multinucleated, active osteoplast that mediate bone resorption. Osteoclast adheres to bone and subsequently remove it by acidification and proteolytic digestion. As the BMU advances, osteoclast leave the resorption site and osteoblast move into cover the excavated area and begin the process of new bone formation by secreting osteoid, which is eventually mineralized in to new bone. After osteoid mineralization, osteoblast flatten and form a layer of lining cells over new bone.5. On completing the cycle (about 120 days), remodeling is balanced if there has been no net change in the amount of bone.3

Blood and nerve supply of the bone:-

One or two nutrient arteries enter the shaft of a long bone obliquely and usually directed away from the growing end. Within the medullary cavity they divided into ascending and descending branches. Near the ends of bone, they are joined by branches from the neighboring systemic vessels and from periarticular vascular arcades. Cortical bone receives blood supply from periosteum and from muscular vessels at their attachment. Vein are numerous and large in the cancellous red marrow bone (e.g. the basi vertebral veins) Lymphatics are present, but scanty; they drain to the regional lymph nodes of the part.

Subcutaneous periosteum is supplied by the nerves of the overlying skin. In deeper parts of the local nerves, usually the branches to nearby muscle provide the supply. Periosteum in all parts of the body is very sensitive. Other nerves, probably vasomotor in function, accompany nutrient vessels into bone.

 

Peak bone mass:-

Peak bone mass (PBM) can be defined as the amount of bony tissue present at the end of the skeletal maturation. The precise age at which peak bone mineral density is a acquired is still unknown and may be site dependent. In general, accepte that up to 90% of peak bone mass is acquired by age 18 in girl and by age 20 in boys, which makes youth the best time to invest in bone health. There after, bone mass increase slightly during the third decade of life and reaches its peak around age 30 years. So, peak bone mass is achieved during adulthood. Its magnitude is determined largely by hereditary factors, especially the allele for the vitamin D receptor molecule. Physical activity, muscle strength, diet, and hormone state however all contribute.26. Factors that may affect peak bone mass- sex, race, genetic factors, gonadal steroids, growth hormone, timing of puberty, calcium intake, exercise, etc.14

Sex and race: White woman have lighter skeletons, than white man or black women, where as black men have the heaviest skeleton.27 The skeleton of Asians appear to be intermediate between those of blacks and whites. In all the three races, women have lower peak bone mass than men. Because initial bone mass is an important determinant of bone mass latter of life, these difference may partially explain observed racial and sexual difference in the incidence of osteoporoses and fractures. However, such generalization should not obscure the fact that some white have high   bone mass, where as individual non-whites may have low bone mass and fracture. Moreover, there seem to be exceptions to the general pattern: Hispanics appear to have hip fracture rate that are even lower than American black. Whereas the Bantu people of South Africa have extremely low fracture rate but also low bone mass. 28

 

Genetic factors: The impact of genetic factors on bone density has been demonstrated in several ways. For example, bone density is lower in daughters of women with osteoporosis than in the daughters of women without osteoporosis. Moreover, the concordance of bone density is much higher among monozygotic twins than dizygotic twins.29 Several genes, including the vitamin D receptor gene, the genes encoding type-1 procollagen, and the estrogen receptor gene, have been implicated in the pathogenesis of osteoporosis, but no conclusive genetic linkages have been demonstrated.14 The type of vitamin D receptor molecule that is inherited accounts for approximately 75% of the maximal peak mass achieved. Polymorphism in the vitamin D receptor or molecule is associated with either a highest or lower maximal bone mass.

Nutrition: Calcium is essential for healthy bone development, and increasing the calcium intake in children and adolescent increase bone growth. Calcium deficiency in young people can account for a 5 to 10 percent different in peak bone mass and can increase the risk for hip fracture latter in life. The skeleton appears to be more responsive to calcium supplementation before the onset of puberty than after puberty has started. It has been shown that adolescent girls (but not boys) have insufficient calcium intake levels in the diet. The calcium deficiency occurs during a period of rapid bone growth, stunting the peak bone mass ultimately achieved; thus, these individual are at greater risk of developing osteoporosis.10 Milk and other dairy products are the most abundant source of calcium. In addition to calcium, protein plays a key role in bone mass acquisition. Besides adequate amount of vitamins C,D,K and minerals such as magnesium, zinc, are also important for bone health. Adolescents with average nutritional calcium intake bellow 1000 mg/day for boys and 850mg/day for girls will probably not reach optimal bone mass. The national osteoporosis foundation describes bone mass as analogous to a bank account in to which, during persons childhood, adolescents, and early adult hood, new bone ‘deposits’ are made to the skeleton faster than old bone is ‘withdrawn’. After the age 30, the rate of withdrawal exceeds the rate of deposit; therefore, establishing healthy bone mass in childhood and early adult hood is crucial.30

Physical activity: girls and boys and young adults who exercise regularly generally achieve greater peak bone mass than those who do not. Physical activity is a determinant of peak bone mass31. Sufficient exercise during childhood and adolescent, particularly the pre pubertal years, is more effective for increasing bone mass and strength than exercise in adulthood. 32  Whether benefits achieved before puberty are sustained into adult hood remains to be determined by appropriate longitudinal studies. In healthy adults, vigorous exercise programs and resistance training of moderate to high intensity can preserve bone density33. Weight bearing physical activity is important for maintenance of bone mass, and activities that increase muscles strength are also safe and beneficial, particularly for bones of the upper limb.34 An optimal, exercise program should include activities for increasing strength, balance, flexibility and coordination of the upper and lower limbs and trunk. To influence BMD, physical activity undertaken 2-3 times per week and maintained for 20 to 60 minutes has been found to be helpful. Training intensity between 70 to 80 % of the functional capacity, or maximum strength can preserve bone density, but remain to be determined whether these are optimal for influencing BMD.35 Low intensity exercise such as walking has minimal effect on BMD.36 In adults, any skeletal benefit accrued from a exercise program will not be sustained, if an individual returns to a secondary life style.32

 

Hormonal factor: sex hormone, including estrogen and testosterone, are essential for the development of bone mass. Beside growth hormone, thyroid hormone, PTH and calcitonin also play crucial roles. The pubertal growth spurt is related to the production of estrogen- the major female hormone. A certain content of body fat may be required to induce the onset of puberty. Adipose tissue mass is correlated tightly with whole body density in women but not in man. This fact brings into focus the notion that dietary indiscretions can have a profound effect on the overall process of fat production, menarche and estrogen protection. Women with eating disorders such as anorexia nervosa or bulimia have diminished body fat as well as abnormalities in menstrual function. These women develop insufficient bone mass either as a result of  loss of bone or as a result of deficient formation.37,38


PATHOLOGICAL BASIS OF LOW BONE DENSITY

 

Definition of osteoporosis: The word osteoporosis is from the Greek osteon for “bone” & porous for “pore” or “passage”.  Indeed osteoporosis literally makes bone more porous. Osteoporosis is a generic term referring to a state of decreased mass per unit volume (density) of normally mineralized bone. Clinically, osteoporosis is synonymous with low bone density. In 1991, a panel of experts arrived at a consensus definition of osteoporosis as a systemic disease characterized by low bone mass and micro architectural  deterioration of the skeleton, leading to enhance bone fragility and increased fracture risk39 This definition encompasses the two important skeletal changes in osteoporosis namely, diminished bone mass and diminished bone quality. However, this is not a practical definition for patient care, because the only means of assessing bone quality (other than fragility fracture) is histologic study of bone biopsy specimens.

The short comings of this definition led the World Health Organization (WHO) to convene a new panel of experts to define just what is meant by the term “low bone mass”40. The group began its deliberations by agreeing on two basic concepts. First, they assumed that fracture risk must be lowest when BMD is highest – sometimes between ages 20 and 40 in healthy people. The relative risk for fracture in this reference group was arbitrarily set at 1.0. Second, the expert panel agreed, on the basis of several studies41 that relative risk for fracture double for each standard deviation (SD) decrement in BMD. Thus, in patient’s in whom BMD is 1SD below the mean for peak bone mass, the relative risk is 2.0. If the value is 2 SD below the mean, the risk double 4.0. The relationship between BMD and fracture risk is continuous, and there is no fracture threshold. With these concepts in mind, the WHO panel developed the following working definitions:-

v         Normal is defined as BMD less than or equal to 1.0 SD below the mean for peak bone mass.

v         Low bone mass (osteopenia) is defined as more than 1.0 but less than or equal to 2.5 SD below the mean.

v         Osteoporosis is defined as more than 2.5 SD below the mean.

These definitions were developed for epidemiologic studies but have been adapted as “Diagnostic Criteria” in much the same way that arbitrarily selected cut points are used to define hypercholesterolemia and hypertension.

 

Prevalence of osteoporosis:– Women of all races and ethnic origin are susceptible to osteoporosis and fracture. But whites, especially of northern European descent, and Asian are at increase risk for osteoporosis., Osteoporosis is not a just a disease of women, and there are compelling reasons for men to join the fight for better access to screening and more equitable reimbursements for screening. Two million of the total 10 million individuals diagnosed with osteoporosis in 1995 were male. Another 3 million men are at risk. Studies completed in 1994 showed that a 50 year old man has a remaining life time risk of osteoporotic fracture of 13% and experiencing such a fracture has more direct implication for man than women: while the rate of hip fracture is two to three times higher in women then men, the one year mortality following a hip fracture is nearly twice as high for men as for women. The statistics paint a chilling portrait of the future for men suffering from osteoporosis. Each year, men suffer 1/3 of all hip fracture that occurs, and 1/3 of these men will not survive more than a year. Over 100,000 men have a hip fracture every year, 1/3 of these men will die of complication from their hip fracture within a year. Of the survivors, more then a quarter will not walk again without assistance. In addition to hip fracture, men also experience painful and debilitating fracture of the spine, wrist, and other bones due to osteoporosis. In type 1 and type 2 osteoporosis, women are affected more than the men, with female to male ratio of 6:2 and 2:1 respectively. In secondary osteoporosis, both sexes are equally affected. The peak incidence of type 1 osteoporosis is in people aged 50 to 70 years, and peak incidence for type 2 is in people aged 70 years or older. Secondary osteoporosis can occur in persons of any age. Accordingly to US census bureau, international database, 2004, 1.45 crore people among 14.13 crore population of Bangladesh are suffering from osteoporosis, which is 10.26 percent of total population. 6.62% patient’s of osteoporosis are under diagnosed world wide and in Bangladesh 0.93 crore are undiagnosed which is 64.13 % of the total osteoporotic patient. Recent National Health and Nutrition Examination Survey (NHANES III, 1988-1994)42 review dual energy x-ray absorptiometry measurements of femoral BMD in a non-Hispanic white population. This snapshot determined peak bone mass in 382 men and 409 women 20 to 29 years of age. According to the WHO criteria, 13% to 18% of women aged 50 or older had osteoporosis, another 37 % to 50% had low bone mass. From the most recent US census data, this translates to 4 to 6 million women with osteoporosis and 13 to 17 million with low bone mass; in men over age 50, the corresponding members are 1 to 2 million with osteoporosis and 4 to 9 million with low bone mass.43 The definition of low bone mass includes persons in whom risk of fracture is at least double that for healthy young adults. Therefore, about 22 million to 34 million Americans aged 50 are currently at increased risk for fracture.

Costs of care: Complication of osteoporosis are major community health problem in terms of both people and healthcare dollars. The estimated cost fractures complicating osteoporosis in 1995 was a staggering $13.8 billion.44  Most of this money ($10.3 billion, or 75%) was spent for treatment of fracture in white women.45 These investigation confirmed the well recognized observation that osteoporosis is principally a problem of ageing white women. Nonetheless, a full 23% of health care expenditures for this disease were incurred by white men (18%) and non-white women (5%). Even the group least susceptible to osteoporotic fracture, non-white men, required $200 million in osteoporosis care in 1995. Most money (63%) went for care of hip fracture, but 37% dollars were spent on other types of fractures. While every effort was made to capture relevant data, fractures other than hip fractures were probably under reported, because most of them do not require hospital admission44.

Morbidity and mortality from hip fractures: Some studies have documented substantial in hospital mortality in patient’s with hip fracture; estimates range from 4% to 11.5%.46 Other studies have shown that this mortality rate remains high for several years after a fracture. In one report, excess in death per 100 cases was 14 during the 5 years after fracture to patient’s who had little functional impairment or low co morbidities before fracture. The fact that the patient’s general health status is important in assessing the risk of mortality after hip fracture is obvious.47

In one study, the 3month mortality was 13.5%, compared with 2.6% in a match Cohort. However, if the fracture occurred in an institution the 3 months mortality was 23%, compared with 10% for institutionalized patient’s who did not sustain a hip fracture. 48

Serving a hip facture is not the end of the study. A Mayo clinic study of men who do had broken hips showed that more than half needed to be discharged to nursing homes. Among those who survived, 97% still resided in nursing homes or in for terminal care facilities or required home health care 1 year later. Only 41% of these men had recovered their pre fracture functional status after 1 year.49 Given this high morbidity and mortality, a great deal of attention has been paid to factors that influence the out comes from hip fractures. The findings are predictable: out come are poorest for patient’s over age 85 years, these with coexisting functional problems, and those with scores of 3 or 4 on the American society of anesthesiologists rating of operative risk. For as yet in unexplained reasons, being male is predictor of unexplained hip fractures that carry a poor prognosis.

Most in hospital death (65%) result from cardiovascular events, and a history of congestive heart failure, angina, or chronic pulmonary obstructive disease contributes substantially to mortality. According to one study, postoperative aspirin administration reduced the risk of dying in hospital by 75%, an important observation that requires additional verification.

In another study of relatively healthily population sustaining hip fracture in their own homes and discharged to their homes, gait and balance were reviewed 2 months after fracture. A 17% increase in 2year mortality was shown for each unit decrease in the balance score (range, 0 to 17), but poor gait were not associated with an increased likelihood of readmission to hospital. However, both poor balance and poor gait ware associated with a substantially increased likelihood of nursing home admission.50

Pathogenesis of osteoporosis:

Skeletal fragility can result from: (a) failure to produce a skeleton of optimal mass and strength during growth; (b) excessive bone resorption resulting in decreased bone mass and micro architectural deterioration of skeleton; (c) an inadequate formation response to increased resorption during bone remodeling. In addition, the incidence of fragility fractures, particularly of the hip and wrist, is further determined by the frequency and direction of falls.

To understand how excursive bone resorption and inadequate formation result in skeletal fragility, it is necessary to understand the process of bone remodeling, which is the major activity of bone cell in the adult skeleton. The bone remodeling or bone mullicellular unit (BMUs) described many years ago by Frost and others51 can occurs either on the surface of trabecular bone as irregular Howship lacunae or in cortical bone as relatively uniform cylindrical Haversian systems. The process begins with the activation of hematopoietic precursors to become osteoclasts, which normally requires an interacuion with cells of the osteoblastic lineage. Because the resorption and reversal phases of bone remodeling are short and the period required for osteoblastic replacement of the bone is long any increase in the rate of bone remodeling will result in a loss of bone mass. Moreover, the larger member of unfilled Howship lacunae and Haversian canals will further weaken the bone. Excessive resorption can also result in complete loss of trabecular structures, so that there is no template for bone formation. Thus, there are multiple ways in which an increase in osteoclastic resorption can result in skeletal fragility. However, high rate of resorption are not always associated with bone loss; for example, during the pubertal growth spurt. Hence an inadequate formation response during remodeling is an essential component of the pathogenesis of osteoporosis.

Central role of estrogen: The concept that estrogen deficiency is critical to the pathogenesis of osteoporosis was based initially on the fact that post menopausal women, whose estrogen level naturally decline, are at highest risk for developing the disease. Morphologic studies and measurement of certain biochemical markers have indicated that bone remodeling is accelerated at the menopause as both markers of resorption and formation increased.52 Hence, contrary to Albright’s original hypothesis, an increase in bone resorption, and not impaired bone formation, appears to be the driving force for bone loss in the setting of estrogen deficiency. But rapid and continuous bone loss that occurs for several years after the menopause must indicate an impaired bone formation response, since in younger individuals going through the pubertal growth spurt, even faster rates of bone resorption can be associated with an increase in bone mass. However, the increased bone formation that normally occurs in response to mechanical loading is diminished is estrogen deficiency, suggesting estrogen is both anticatabolic and anabolic.53

Estrogen deficiency continues to play a role in bone loss in women in their 70 s and 80s, as evidenced by the fact that estrogen treatment rapidly reduces bone breakdown in these older women. More over, recent studies in humans have shown that the level of estrogen required to maintain relatively normal bone remodeling in older post menopausal women is lower than that required to stimulate classic target tissue such as the breast and uterus. Fracture risk is inversely related to estrogen level in post menopausal women, and as little as one-quarter of the dose of estrogen that stimulate the breast and uterus is sufficient to decrease bone resorption and increase bone mass in older women. This greater sensitivity of the skeleton may be age related.54

Estrogen is critical for epiphyseal closure in puberty in both sexes and regulates bone turnover in men as well women. In fact, estrogen has a greater effect than androgen in inhibiting bone resorption in men; although androgen may still play a role.55 Estrogen may also be important in the acquisition of peak bone mass in men. Moreover, osteoporosis in older men is more closely associated with low estrogen than with low androgen levels.56

Estrogen deficiency increases and estrogen treatment decreases, the rate of bone remodeling, as well as the amount of bone lost with each remodeling cycle. Studies in animal models and in cell culture have suggested that this involves multiple sites of estrogen action, not only on the cells of the BMU but on other marrow cells. Estrogen acts through 2 receptors: Estrogen receptor  (ER) and ER . ER appears to the primary mediator of estrogen’s actions on the skeleton.53 Osteoblast do express ER but actions of ER agonist on bone are less clear. Some study suggest that the effect of estrogen signaling through ER and ER are in opposition, while other study suggest that activation of this two receptors has similar effects on bone.57

Single nucleotide polymorphisms (SNPs) of ER may affect bone fragility. In largest study to date, 1 of the SNPs for this receptor was associated with a significant reduction in fracture risk, independent of bone mineral density (BMD). Other studies have suggested that SNPs of ER can affect BMD and rates of bone loss as well as fracture risk in both men and women.58

An orphan nuclear receptor, estrogen receptor related receptor  (ERR), with sequence homology to ER and ERR, is also present in bone cells.59 Despite its inability to bind estrogens, this receptor may interact with ER and ER or act directly to alter bone cells function. A regularly variant of the gene encoding ERR was recently found to be associated with a significant difference between lumbar spine and femoral neck BMD in premenopausal women.60

Sex hormone-binding globulin (SHBG), the major protein for sex steroids in plasma, may not only alter the bioavailability of estrogen to hormone-responsive tissues but also affect its entry in to cells. Epidemiologic studies suggest that SHBG may have a effect on bone loss and fracture risk independent of the effect as a binding protein.61

While estrogen can act on cells of the osteoblastic lineage, its effect on bone may also be dependent on actions on cell of the hemotopoietic lineage, including osteoclast precursors, mature osteoclasts and lymphocytes. Local cytokines and growth factors may mediate these effects. The effects of estrogen on cytokine production may be mediated by T cells.  A direct effect of estrogen in accelerating osteoclast apoptosis has been attributed to increased TGF- production.62

Calcium, Vitamin D, and parathyroid hormone:

The concept that osteoporosis is due to primarily to calcium deficiency particularly in the elderly, was initially put forward as a counter proposal to Albright’s estrogen deficiency theory. Decreased calcium intake, impaired intestinal absorption of calcium, due to aging or disease, as well as vitamin D deficiency can result in secondary hyperparathyroidism.  The active hormonal form, 1, 25, dihydroxy vitamin D (calcitriol), is not only necessary for optimal intestinal absorption of calcium and phosphorus, but exerts atonic inhibitory effect on parathyroid hormone (PTH) synthesis, so that there are dual path ways that can lead to secondary hyperparathyroidism.63 Vitamin D deficiency and secondary hyperparathyroidism can contribute not only to accelerated bone loss and increasing fragility, but also to neuromuscular impairment that can increase the risk of fall.64 Clinical trial involving older individuals at high risk for calcium and vitamin D deficiency indicate that supplementation of both can reverse secondary hyperparathyroidism, decrease bone resorption, increase bone mass, decrease fracture rate, and even decrease the frequency of falling.63 However, in a large recent study, calcium and vitamin D supplementation did not reduce fracture incidence significantly, perhaps because this population was less deficient in Vitamin D.65

Polymorphisms of the VDR have been studied extensively, but the results have been variable. This may be in part because the effect of a given polymorphism in this receptor is dependent on an interaction with the environment, particularly with calcium.66 VDR polymorphism are also associated with deficiency in the response to therapy with calcitriol.67 There is also evidence for an effect on fracture risk independent on bone density and bone turnover, which might be due to an alteration in the frequency of falls.68

Secondary hyperparathyroidism present when there is relative insufficiency of vitamin D, that is, where the level of circulating form-25- hydroxy vitamin D- fall below 30ng/ml, suggesting that the target for vitamin D supplementation should be at this level or higher.69 The seasonal decrease in fractures, independent of the increase in rate of falls.70 In addition, increase PTH level are associated with increased mortality in the frail elderly, independent of bone mass and vitamin D status. The precise mechanism underlying this relationship have not yet been determined, but the risk of cardiovascular death was increased.71 Polymorphism of the calcium sensing receptor, which regulates calcium secretion by suppression of PTH translation and PTH secretion, have not yet been associated with any alteration in bone phenotype.

Receptor activator of NF-, its ligand, and osteoprotegerin:

The concept that stimulation of bone resorption requires an interaction between cells of the osteoblastic and osteoclastic lineages was put forward many years ago, but its molecular mechanism was only identified recently.72 Three members of the TNF and TNF receptor super family are involved; Osteoblast produce RANKL, a ligand for receptor activation of NF-B (RANK) on haemopoietic cells, which activates the differentiation of osteoclasts and maintain their function. Osteoblasts also produce and secrete osteoprotegerin (OPG), a decoy receptor that can block RANKL/RANK interactions. Stimulators of bone resorption have been found to increase RANKL expression in osteoblasts, and some also decrease OPG expression.73 Bone cell appear to express the membrane-bound form of RANKL, and thus, osteoblasts must physically interact with osteoclasts precursors in order to activate RANK. Soluble RANK can be produced by activated T lymphocytes and is as active as membrane-bound RANKL in binding to RANK.74 Recently a monoclonal antibody against RANKL was shown to produce prolonged inhibition of bone resorption in post menopausal women.75 It was also shown that RANKL level were increased on the surface of bone marrow cells for early post menopausal women who were estrogen deficient.76 However, it has been difficult to demonstrate a role for OPG deficiency in the pathogenesis of osteoporosis. Since OPG levels are not consistently altered, OPG level increase with age, and it is possible that OPG production rises as a homeostatic response to limit the bone loss that occurs with an increase in other bone resorbing factors.77 Polymorphism in the OPG gene have been associated with osteoporotic fracture and differences in BMD.78 OPG Polymorphisms have also been linked to coronary artery disease.79

The RANKL/RANK interaction is critical for both differentiation and maintenance of osteoclast activity and hence represents a final common pathway for any pathogenetic factor in osteoporosis that acts by increasing bone resorption, while it is assumed that cells of the stromal / osteoblastic lineage are the major source of RANKL in physiologic bone remodeling, other cells may act as a source of RANKL in pathologic states; for example, T cell production may play a role in osteoporosis as well as inflammatory bone loss. 80

Recently a second system that might affect the interaction between osteoblast  and osteoclast has been identified.81 This involves the membrane adapter DNAX-activating protein 12 and Fc receptor common chain. Deletion of this molecule results in severe osteoporosis in mice. The molecules are involved in signaling through the immunorecptor tyrosine-based activation motif (ITAM). Co-operation between RANKL and ITAM signaling may be essential for osteoclastogenesis, for which nuclear factor of activated T cells (NFAT) is the master transcription factor.

 

Genes determining osteoblast differentiation and function:

Recent discoveries of signal transduction pathways and transcription factors critical for osteoblast differentiation and function have opened up new approaches to understanding the pathogenesis of osteoporosis. Gene deletion studies have shown that absence of runt-related transcription factor 2 (Runx2) or a downstream factor, osterix, are critical for osteoblast differentiation.82 Interestingly, over expression of Runx2 leads to a decrease in bone mass. 83 A role for polymorphism of these transcription factors in osteoporosis had not yet been identified.

The recent identification of the critical role for the Wnt signaling pathway in regulating osteoblast function is of particular interest, since it has been shown to play an important role in determining bone mass and strength. LDL-receptor-related protein 5 (LRP5) interacts with the frizzled receptor to transduce signaling by Wnt ligands. A mutation of LRP5 that leads to constitutive activation can result in an increase in bone density.84 The phenotype of families with LRP5 activating mutations varies considerably, although all show a striking absence of fractures. Some have normal skeletal structure, while others show abnormalities due to skeleton overgrowth.85 Deletion of LRP5 results in a severe osteoporotic syndrome associate with abnormal eye development.86 Polymorphism of LRP5 have been associated with differences in bone mass and fractures.87 Mutation of LRP5 have been identified in a few patient’s with idiopathic juvenile osteoporosis.88 However, Wnt signaling it also critical in bone development and can affect peak bone mass. 89 The inhibition of skeletal growth by glucocorticoids may be mediated by effects Wnt signaling. The precise mechanism whereby Wnt signaling alters osteoblast function are not fully understood, but there is evidence that the canonical-catenin pathway is involved and that there is an interaction with bone morphogenetic protein 2 (BMP2).90 There are a number of inhibitors that have been shown to interact with BMP2 and with the Wnt signaling pathway. One of these, Sclerostin, the product of the SOST Gene, has been shown to inhibit both BMP2 and Wnt signaling. Another potential inhibitory factor is the production of secreted frizzled-related protein (SFRP) by osteoblasts.91

Local and systemic growth factor:

Remodeling imbalance, characterized by an impaired bone formation response to increased activation of bone remodeling, is an essential component of the pathogenesis of osteoprosis.92 This may be due, in part, to an age-related decrease in the capacity of osteoblasts to replicate and differentiate. However, it seems likely that specific defects in the production or activity of local and systemic growth factor which also contribute to impaired bone formation BMPs as well as other members of the TNF family have been implicated. IGF, which is both a systemic and local regulator, as well TGF-, can also alter bone formation. There are some association between BMD and the incidence of the osteoporotic fracture and polymorphisms in the genes encoding IGF-1 and TGF-.93 But the largest study to date, in Icelandic and Danish Cohorts, suggests that polymorphisms of the BMP2 gene are linked to low BMD and fracture risk.94 Inhibition of local IGF-1 production may be an important component of glucocorticoid- induced osteoporosis as well as inhibition of growth in childhood.95

Cytokines, prostaglandin’s, NO, and leukotrienes:

The concept that locally produced cytokines such as IL-1 and prostaglandin such as prostaglandin E2 (PGE2) can affect bone in more than 30 years old.96 Subsequently, many cytokines were found to either stimulated or inhibits bone resorption and formation.97 Prostaglandins have both stimulatory and inhibitory actions; however, the predominant effect of PGE2, which is the major prostaglandin produced by bone cells, is to stimulate both resorption and formation.98 The possibility that these factors might also be involved in the pathogenesis of osteoporosis is based largely on animals studies of bone loss after ovariectomy.99 However, there is evidence that polymorphisms of IL-1, IL-6, TNF- and their receptors can influence bone mass in human.100

Postaglandins, particularly PGE2, are produced by bone cells largely through the action of inducible cyclooxygenase 2 (COX2). COX2 is induced by most of the factors that stimulates bone resorption and thus may enhance the response to these agents.98 Treatment with COX-2 inhibitor blunt the response to impact loading and fluid shear stress, indicating that prostaglandins play an important role in the response of mechanical forces, and this may be enhanced by estrogen,101 In epidemiologic studies, small increases in BMD and decrease in fracture risk have been reported in individuals using NSAIDS, 102

NO is produced by bone cells and is a cofactor for the anabolic response to mechanical loading.103 However, unlike prostaglandins, NO may inhibit bone resorption, perhaps by increasing OPG production.104 This effect may be responsible for the increase in BMD that has been demonstrated in patient’s treated with isosorbide mononitrate and other activators of the NO pahway.105

Leukotrienes, the products of lipoxygenase, can affect bone by stimulating resorption and inhibiting formation.106 Recently, arachidonate15-lipoxygenase, was identified as a negative regulator of bone density in mice,107 and polymorphisms in the human gene, ALOX15, were found to be associated with differences in peak BMD in postmenopausal women. 108

Collagen abnormalities:

A Polymorphism of the first intron of the gene coding for the type 1 collagen 1 chain and increased level of homocysteine can influence fracture risk independent of BMD.109 This may be due to differences in helix formation or cross-linking of collagen, challenging the concept that mineral and matrix composition are normal in osteoporosis and that only structural abnormalities account for skeletal fragility.

Leptin and neural pathways:

Leptin deficiency or resistance is associated with high BMD in mice despite the fact that gonadal function is diminished.110 This has been attributed to a central effect on adrenergic signaling. Increased  adrenergic activity can decrease bone mass, but other neural pathways may be involved.111 Some, but not all, epidemiologic studies suggest that -adrenergic blockers can decrease fracture risk and increase BMD.112 Another neural pathway has recently been implicated by the finding that mice in which the canabinoid  type-1 receptor is activated, as well as mice treated with antagonist of this receptor, are protected from ovariectomy-induced bone loss.113

Risk factors for low BMD:      

Bone mass reflects the mass accumulated during growth, less any bone mass that has been lost since the adult peak was attained. A strong genetic component is apparent in peak bone mass. In addition, maximum bone mass is influenced by diet (calcium, protein) and exercise. Children with many disease or condition that interferes with growth, nutrition, and exercise have suboptimal bone mass. Recent studies suggest that use of long-acting contraceptives, such as medroxyprogesterone acetate, may limit skeletal growth during puberty, but this observation requires confirmation.114

In women, BMD is stable from the mid-20s to the earliest stages of the climacteric and then declines as estrogen production falls. In men, the timing and mechanism of normal bone loss are less well understood. Many circumstances shorten the time during which peak BMD is stable (table-1). Most of these are not influenced by changes in diet and life style alone, which is an important difference between osteoporosis and hypertension on hypercholesterolemia. Exceptions are cigarette smoking,115 and excessive use of alcohol, which have adverse effect on skeleton as well as on most other organ systems. Each of the circumstances listed in the table has an impact on the skeleton at any time in life. The effect is aggravated if coupled with lower estrogen level after menopause.

Table-1 Disease and conditions associated with low bone mass

Hormone excess

Parathyroid hormone, primary and secondary

Thyroxin, endogenous and exogenous

Cortisol, endogenous and exogenous

Hormone deficiency

Estrogen, premenopause (may be linked with anorexia, bulimia, athletic amenorrhoea, premature menopause, prolactinoma, hypopituitarism)

Estrogen, postmenopause

Testosterone, primary and secondary testicular failures.

Vitamin D metabolites, inadequate intake or malabsorption

Miscellaneous (not necessarily mediated by hormonal abnormalities)     

Medical conditions

v  Gastrectomy

v  Idiopathic hypercalciuria

v  Systemic mastocytosis

v  Prolonged immobilization (paraplegia, quadriplegia)

Lifestyle factors

v  Cigarette smoking

v  Excessive ingestion of caffeine

v  Excessive sodium intake (promotes hypercalciuria)

Medications

Heparin, warfarin, cyclosporine

One condition that requires special mention is idiopathic hypercalciuria in a patient with a calcium containing kidney stone. The ‘reflex’ response is to restrict dietary calcium intake so urinary calcium excretion declines and the risk of additional stone formation falls. This is not necessarily a good idea, since many such patient’s have a renal calcium leak that is not influenced by diet. This renal leak promotes a negative calcium balance, and the skeleton pays the price in an attempt to preserve balance. Eliminating calcium from diet exacerbates the negative calcium balance and further compromises the skeleton.

Corticosteroids are best known of the medications that decrease BMD. Long term experience with inhaled Corticosteroids does not yet confirm that they are less detrimental to the skeleton than other Corticosteroids, but initial studies suggest this might be the case.116

Thyroid disease also can cause problems with bone mass. Many women are receiving thyroid replacement therapy for hypothyroidism, which is appropriate if the disease is well documented and if replacement is not excessive (ie, serum thyrotropin level remains within the normal range and is not suppressed). Otherwise, chronic mild, symptomatic iatrogenic hyperthyroidism probably increases bone loss, and long-term overmedication with thyroxin result in low BMD.

 

Other risk factors for fracture:

A history of fracture, apparently even traumatic fractures before menopause but especially low-impact fractures after menopause, substantially increase the risk.117 A family history of fragility fractures (after trauma equal to or less than a fall from a standing height) is a significant contributory to fracture risk. Given the scant attention paid to osteoporosis until recently, this information is often missing from or incorrect in the patient history.

Body habitus is also an important factor in hip fracture risk with fractures being more than twice as likely in women 5ft 8in, or taller than women 5ft 2in, or shorter.118 the corresponding heights for men are 6ft and 5ft 9in.119

 

Women in the lowest quartile for body weight are also at increased risk for fracture, whilewomen who gained weight after age 25 are at lower risk of fracture.120

Iatrogenic hip fractures probably occurs, and the risk increases with use of long acting benzodiazepins.121 On the positive side, reasonable evidence suggests that thiazide diureric therapy offers some protection against hip fractures in elderly patient’s.122 This does not imply that thiazides should be prescribed to treat osteoporosis or prevent hip fractures. However, if a diuretic is indicated is a patient at risk for fracture because of age and low bone density, thiazides should be considered.

The high incidence of vitamin deficiency, even in the well elderly in the United States, is receiving a great deal of attention.123 A prospective, controlled study in France showed that daily supplementation with 100 mg of calcium and 800IU of vitamin D significantly decrease the incidence of hip fracture in a nursing home population. Whether this occurs through an effect on BMD or because of the known beneficial effects of vitamin D on striated muscle was not established. This investigation did demonstrate that the supplements corrected mild hyperparathyroidism. 124

Other studies have shown that a high rate of bone turnover may be associated with an increased hip fracture risk independent of BMD. The effects of high bone turnover and low BMD were additive in terms of risk fracture. Thus, it would seem cost effective to provide 1,000 mg of calcium and 800 IU of vitamin D daily to everyone in the United States age 75 or older.125, 126

Many simple, objective measures of frailty can help assess the risk of hip fracture. These include ability to rise from a chair without use of the arm, depth perception, contrast sensitivity, and gait and balance assessment. Simply put, any condition that increase the risk of falling in the elderly increase the risk of fracture.127

Types of osteoporosis: 

Osteoporosis may be either a primary or a secondary form. Primary osteoporosis is the more common form and due to the typical age related loss of bone from skeleton. Primary osteoporosis is classified as type-1 and type-2. Secondary osteoporosis results from the presence of other disease or conditions that predispose to bone loss and is classified as type-3.

Type-1: Type-1 or postmenopausal osteoporosis occurs in 5% to 20% women, affecting those within 15 to 20 years of menopause,128 with a peak incidence in the 60s and early 70s. The incidence in women is eight times higher than that in men.129 The frequency of postmenopausal osteoporosis accounts for the overall female-male ratio of 2 : 1 to 3 : 1.

Estrogen deficiency is thought to underlie this from of osteoporosis, rendering skeleton more sensitive to parathyroid hormone (PTH) resulting in increased calcium resorption from bone. This in turn decreases PTH secretion, 1-25 -dihydroxy-vitamin D production, and calcium absorption and ultimately causes loss of trabecular bone, leading to vertebral crush fracture and colles’ fracture.

Women can loss around 2% to 3% of their bone per year for the first 5 years after menopause. Because of the low estrogen production, women loss nearly 50% of their trabecular bone and 35% of their cortical bone through their life time, whereas men loss only 25% of both types of bone. At least 75% of bone loss that occurs in women during the first two decades after menopause can be attributed to lack of estrogen rather than aging. Bone loss associated with menopause dose not begins with the onset of amenorrhoea but may occur 1 to 3 years before the actual cessation of menstrual periods.130

Type-2: Type-2 osteoporosis or senile osteoporosis occurs in women or men more than 70 years of age and usually is associated with decreased bone formation along with decreased ability of the kidney to produce1,25,(OH)2D3. The vitamin D deficiency results in decreased calcium absorption, which increases parathyroid hormone (PTH) level and therefore, bones resorption. In type-2 osteoporosis, cortical and trabecular bone is lost, particularly leading to increased risk of hips, long bones, and vertebral fractures.

Type-3: Type-3 or secondary osteoporosis occurs equally in men and women and at any age. In men, most cases are due to disease or to drug therapy, but in 30% to 45% of affected individuals no cause can be identified.131 In various series of osteoporotic patient’s, secondary osteoporosis accounts for about 40% of the total number of osteoporotic fracture seen by a physician.132

This type of osteoporosis is associated with variety of conditions, including hormonal imbalance (eg. Cushing’s syndrome); cancer (notably multiple myeloma); gastrointestinal disorders (especially inflammatory bowel disease causing malabsorption); drug use (eg. corticosteroid, cancer chemotherapy, anticonvulsants, heparin, barbiturates, valproic acid, gonadotrophin-releasing hormone (GnRH), excessive use of aluminum containing antacids); chronic renal failure; hypothyroidism, hypogonadims in men; immobilization; osteogenesis imperfecta and related disorder; inflammatory arthritis (particularly Rheumatoid arthritis); and poor nutrition (including malnutrition due to eating disorders).133, 134, 135


CLINICAL PRESENTATION OF LOW BONE DENSITY

 

Symptoms:

Osteoporosis is a clinically silent but progressive disease until fracture occurs. Since low bone density alone dose not cause symptoms, many patient’s with quite advanced osteoporosis remain asymptomatic until a fracture occurs. These fractures typically affect the forearm (Colles’ fracture), spine (vertebral fracture) and femur (hip fracture). Colles’ fracture and vertebral fracture most often occurs in women age 55 and above, where as hip fracture affect older individuals (aged 70+). Osteoporotic limb fractures are usually precipitated by falls, where as the precipitating factor in vertebral fracture is often being lifted or lifting a heavy weight. The clinical presentation of vertebral fracture is highly variable. Common clinical presentation include; increasing dorsal kyphosis (Dowager’s hump), loss of weight and back pain. Skeletal back pain may also be a symptom. Radiograph may show osteopenia. This finding indicates that at least 30% of bone mass has been lost.

Assessment:

The assessment of osteoporosis should include a through medical history to identify risk factor for low bone density and fracture, routine laboratory test to rule out secondary causes, a physical examination to identify signs and symptoms of fractures, and bone mineral density (BMD) testing.

History and physical examination:

The history and physical examination are neither sensitive enough nor sufficient for diagnosing primary osteoporosis. However, they are important in screening for secondary forms of osteoporosis and directing the evaluation. A medical history provides valuable clues to the presence of chronic conditions, behaviors, physical fitness, and the long term use of medications that could influence bone density.

Those already affected by complications of osteoporosis may complain of upper or mid thoracic back pain associated with activity, aggravated by long periods of sitting or standing, and easily relived by rest in the recumbent positions. The history should also assess the likelihood of fracture. Low bone density, a propensity to fall, grater height and prior fracture are indications of increased fracture risk.

The physical examination should be through for the same reasons. For example, lid lag, and enlargement or nodularity of the thyroid suggests hyperthyroidism. Moon faces, thin skin and buffalo hump suggest Cushing’s syndrome. Cachexia mandates screening for an eating disorder or malignancy. A pelvic examination is necessary for the complete evaluation of women. Osteoporotic fractures are a late physical manifestation. Common fracture sites are vertebrae, forearm, femoral neck, and proximal humerus. The presence of a Dowager’s hump (Spinal curvature) in elderly patient’s indicates multiple vertebral fractures and decreased bone volume.

Complications:

Vertebral fracture, a well recognized complication of osteoporosis, is the most common osteoporotic fracture. Less than one third of these fractures are clinically identified. Regardless of whether they are symptomatic or identified on imazing, vertebral fractures are associated with increased mortality and morbidity rates. Complications include back pain and decreased mobility, with consequent days of bed rest. Compression fracture of the vertebrae varies in degree from mild wedges to complete compression.

Disfiguring kyphosis (Dowager’s hump) is usually related to multiple wedge fracture of the dorsal vertebrae. Abdominal protrusion, which occurs as consequences of the kyphosis is an unrecognized aspect of osteoporosis. Height loss occurring as a consequence of vertebral fractures is one of the most distressing aspects of osteoporosis in many women.

Decreased pulmonary capacity is a known complication of kyphosis; if severe, this may lead to shortness of breath and pulmonary symptoms of restrictive lung disease. Also, the incidence of esophagitis is increased in patient’s with kyposis because of changes in the abdominal cavity. Once vertebral fracture occurs, the process may be relentless with ongoing further vertebral fractures and height loss despite correction of BMD. 136, 137

 

 

Differential Diagnosis:

Endocrinologic diseases

Endocrinologic deceases include the following.

  • Hypogonadism in men and women.
  • Cushing’s syndrome
  • Corticosteroid –induced osteoporosis
  • Hyperthyroidism.
  • Severe primary hyperparathyroidism

In patient’s with acromegaly, the effects of growth hormone excess on bone mass are controversial. Some studies show increase bone mass, and some studies show reduced bone mass. The latter findings may reflect accompanying hypogonadism, a frequent finding in acromegaly. However the data about bone mass and fracture in diabetes, acromegaly and endometriosis are conflicting.

A rare form of osteoporosis occurs during pregnancy or shortly after delivery. The presentation usually includes severe back pain and multiple vertebral fractures. About 70% of cases occur in first pregnancies, and recurrences are unusual. Most cases resolve spontaneously, and bone mass increases after the termination of breastfeeding. In many women, bone mass normalizes after 3 years. Only a small number of patient’s are disabled for months or years. Patient’s with osteoporosis of pregnancy are at increased risk for postmenopausal osteoporosis.

Osteoporosis occurring late in pregnancy may be related to poor diet or calcium and vitamin D deficiency, where as cases occurring during lactation seem to be related to excessive secretion of PTH-related peptide, which is responsible for calcium transport in the breast and for the mobilization of calcium from bone to milk.

 

Nutritional Deficiencies:

Nutritional deficiencies affect the skeleton by impairing the supply of calcium and vitamin D, leading to secondary hyperparathyroidism and osteomalacia. Such deficiencies can occur after gastric resection and in patient’s with short- bowel syndrome. In those with anorexia nervosa, nutritional deficiency is exacerbated by amenorrhea.

Immobilization:

Immobilization, either temporary or from permanent neurological deficit may cause bone loss from disuse.

Medication use:

Long term corticosteroid use constitutes the most common form of secondary osteoporosis in both men and women. Corticosteroids cause impaired osteoblast function and changes in calcium homeostasis, which lead to accelerated bone loss and fracture. In patient’s treated with prednisolone doses exceeding 7.5mg/d for more than 6 months, the prevalence of vertebral fracture 30-50%.

Agonist of gonadotropin-releasing hormone reduces circulating estrogen levels and thereby causes excessive bone loss. In premenopausal women, tamoxifen and Raloxifene interfere with the binding of estradiol to nuclear receptors and thereby impair the cellular action of the hormone.

In vitro experiments have shown that heparin reduces osteoblastic activity and decreases osteoblast adhesion to matrix proteins. Long-term treatment with heparin is a known cause of osteoporosis.

Both aluminum and lithium interfere with intracellular signaling, and aluminum also impairs osteoblast function and causes osteomalasia. Antiepileptic drugs, especially phenytoin, have been shown to interfere with vitamin D metabolism and to increase the risk of osteoporotic fractures.

 

Juvenile osteoporosis:

This type of osteoporosis affects children and is therefore unlikely to be confused with involutional osteoporosis. Juvenile osteoporosis is characterized by the occurrence of primarily vertebral and metaphysial fractures that lead to back pain and difficulty in walking. In most publications, boys are predominantly affected, but most children recover fully.

The National Institutes of Health (NIH) consensus Development Panel on Osteoporosis prevention, Diagnosis, and Therapy asserts that secondary causes of bone loss are more common in men and perimenopausal women than in postmenopausal women. According to the panel’s estimates, secondary cause are responsible for 30% to 60% of osteoporosis in men (mostly due to hypogonadism, glucocorticioid use, and alcoholism) and more than 50% of osteoporosis in perimenopausal women (mostly due to hypoestrogenemia, glucocorticoid use, excessive levels of thyroid hormone, and anticonvulsant use).138

Laboratory Test:

Basic chemical analysis of serum is indicated when the history suggests other clinical conditions influencing the bone density. The tests presented in tables2139 and 3140 are appropriate for excluding secondary causes of osteoporosis.139 These tests provide specific clues to serious illness that may otherwise have gone undetected and which, if treated, could result in resolution or modification of bone loss. Specific biochemical markers (human osteocalcin, bone alkaline phosphatase, immunoassays for pyrinoline cross-links and type 1 collagen-related peptides in urine) that reflect the overall rate of bone formation and bone resorption are now available. These markers are primarily of research interest and are not recommended as part of the basic workup for osteoporosis. They have a high degree of biologic variability and diurnal variation and do not differentiate causes of altered bone metabolism.141-143

For example, measures of bone turnover increase and remain elevated after menopause but do not necessarily provide information that can direct management.

Table-2

Evaluation of secondary osteoporosis

Abnormal study result

Suggested pathology

Increased creatinine level Renal disease
Increased hepatic transaminase level Hepatic disease
Increased calcium level Primary hyperparathyroidism or malignancy
Decreased calcium level Malabsorption, vitamin D deficiency
Decreased phosphorus level Osteomalacia
Increased alkaline phosphatase level Liver disease, Paget’s disease, fracture, other bone pathology.
Decreased albumin level Malnutrition
Decreased TSH level Hyperthyroidism
Increased ESR Myeloma
Anemia Myeloma
Decreased 24 hour calcium excretion level Malabsorption, vitamin D deficiency
TSH= Thyroid stimulating hormone; ESR= erythrocyte sedimentation rate.

Table-3

Direct laboratory assessment for secondary osteoporosis

Cause

Finding/test

Hypogonadism Decreased testosterone level in men

Decreased estrogen level in women

Increased gonadotropin level (LH and FSH)

Hyperthyroidism Decreased TSH level

Increased T4 level

Hyperparathyroidism Increased parathyroid hormone level.

Increased serum calcium level.

Increased 1, 25, hydroxyvitamin D level

Vitamin D deficiency Decreased 25- hydroxy calciferol level
Hemochromatosis Increased serum iron level

Increased ferritin level.

Cushing’s syndrome 24 hours urine free cotisol excretion

Over night dexamethason suppression test

Multiple myeloma Serum protein electrophoressis-M spike and Bence Jones proteinuria

Increased ESR

Anemia

Hypercalcemia

Decreased parathyroid hormone

LH=luteinizing hormone; FSH= Follicule- stimulating hormone; TSH= thyroid- stimulating hormone; T4= thyroxin; ESR= erythrocyte sedimentation rate.

Methods for BMD measurement:

BMD is determined by measuring the amount bone mineral (calcium hydroxyapatite) per unit volume of bone tissue. X-rays or gamma rays are offen use to quantify BMD. In quantitative terms, BMD is the amount of calcium hydroxyapatite, or Ca10 (PO4)6(OH) 2, perunit volume of bone tissue examined.

Common methods conventional radiography, quantitative CT (QCT), single- photon absorptiometry (SPA), dual-photon absorptiometry  (DPA), quantitative ultrasonography (QUS), and dual-energy X-ray absorptiometry (DEXA).

Bone density measurements can be performed by using X-ray methods, such as DEXA, QCT, and ultrasonic methods. The most accurate way to diagnosis osteoporosis is by measuring bone mass. DEXA scans can be used to detect small changes in bone mass by comparing the patient’s bone density to that of healthy adults (T score) and to age-matched adults (Z score).

A number of methods have been developed for the in vivo determination of bone density in patients at risk of osteoporosis. Two of the most frequently used methods are based on measuring the attenuation of a beam of electromagnetic radiation or ultrasound when it passes through the bone. Ultrasonic measurement of velocity through the bone has also been used to determine bone density.

Currently, DEXA is the most accurate and recommended method for BMD measurement. It is a sensitive technique and can detect changes in bone density only 6-12 months after a previous measurement is obtained. Density measurements of the spine or hip are used. The procedure takes approximately 20-30minutes. The radiation exposure is low at approximately 2.5 mrem.

Bone biopsy may be useful in unusual forms of osteoporosis, such as osteoporosis in young adults. Biopsy provides information about the rate of bone turnover and the presence of secondary form of osteoporosis, such as myeloma and systemic mastocytosis. Patient’s with high turnover usually respond better to antiresorptive drugs than other treatments. Bone turnover can also be evaluated by estimating certain biochemical markers, such as osteocalcin and deoxypyridinoline.144

X-ray (plain x- ray):-

Conventional radiographs are relatively insensitive for demonstrating osteoporosis. At least 30% of the bone mass must be lost before it is recognized. At this stage, the radiographic changes of generalized osteoporosis are more prominent in the axial skeleton than elsewhere.

In the spine, the accentuated primary trabecular pattern produces a vertically striated appearance in the vertebral bodies. Likewise, the loss of trabecular mass causes accentuation of the cortical outline, which is described as picture framing of the vertebral bodies. The vertebral bodies may develop a biconcave shape or compression fractures. In trabecular bones, the loss of   trabecular bone may cause the metaphyses to appear radiolucent. Pathologic fractures may occur at multiple sites.

In trabecular bones, bone resorption may be distinguished in 3 sites: endosteal   envelope, intracortical (Haversian) envelope, and periosteal envelope. These changes are best depicted with magnification radiography and quantitated with radiogrametry.

Other radiographic manifestation of osteoporosis includes the following:

–          Involvement of the lower dorsal and lumber spine, proximal humerus, femoral neck, and ribs (These sites are most commonly affected).

–          Increased radiolucency of bones

–          Decreased number and increased thickness of trabeculae

–          Cortical thinning

–          Juxtra- articular osteopenia with trabecular prominence

–          Bone bars (reinforcement lines)

–          Insufficiency fractures

–          Vertebral wedge fractures, fish vertebrae, decreased heights of vertebrae and accentuation of the cortical outlines (also called picture framing)

The assessment of a reduced radiological shadow density varies from physician to physician. So, the sensitivity and reliability of standard radiography to assess BMD are poor and as a result, this technique can not be used to diagnose osteoporosis. Radiography of the thoracic and lumbar spine is indicated only to identify and confirm the presence of fracture or to exclude possible metastasis.145

QCT Scan (Quantitative Computerized tomography):

QCT is generally used to measure bone density in the lumbar spine, though it can be applied to other parts of the skeleton, such as the forearm. The accuracy and scanning time depends on the type of CT scanner used. This technique is the only BMD-measurement method to provide a true volumetric measurement of bone density (in milligrams/cubic centimeters) and a separate measurement of trabecular and cortical bone density.

QCT has been used to assess vertebral fracture risk. It has been found to be superior to other methods for assessing age-related bone loss, for distinguishing fractures, and for diagnostic classification.

Recent development in the CT technology allows 3-dimensional (3D) Volumetric BMD analysis of the proximal femur and high-resolution CT (HRCT) allows the analysis for trabecular structure. QCT bone density measurement of the lumber spine can be performed on standard CT scanners with provision of specialized software, and peripheral QCT measurement can be obtained on specially designed small-bore CT scanners.

The measurements are accurate and precise and require a comparatively low radiation dose in comparison with that needed for a standard diagnostic CT procedure. QCT is more accurate than DEXA in measuring BMD, especially in the spine in the older population group, as CT avoids the effect of degenerative disease and extraneous calcification. Resent development in 3D QCT allows assessment of the hip and complicated situation in the spine, as when both scoliosis and vertebral fracture are present.

False positives/negatives: One major disadvantage of QCT is that artifacts hamper the CT data, reducing its accuracy. The usual sources of error include beam hardening, detected scatter, and system drift. The accuracy of QCT reading can be improved with careful attention to detail. Patient’s should be well centered and scanned by using consistent settings. Another limitation of QCT is a significantly higher radiation dose than that of DEXA.

The presence of excess fat in the marrow in trabecular bone in aging population introduces an error in the BMD measurement of 7-15% per 10% of fat. This problem can be resolved by using dual energy, but at the expense of double the radiation exposure to the patient. The accuracy error and precision of QCT are 5-8%.146, 147

SPA (Single photon absorptiometry) Study: –

SPA was established in 1963 for the bone densitometric evalution of the appendicular skeleton. SPA uses a single-energy source of gamma rays (iodine 125; photon energy, 27.3 keV) or Am-241 (60keV) to produce a collimated pencil beam, which is tracked across the measurement site. The half-life of 125I is approximately 60 days, resulting in a useful life of around 6 months. The transmitted photons are counted by using a sodium iodide crystal/photomultiplier for each point along the track.

Because of the low photon flux and energy source, the technique is usually applied to a peripheral skeletal site, such as the forearm and, less commonly, the heel. The forearm chosen is the nondependent arm. To allow correction for soft tissue, the forearm must be placed in a water bath. The mean photon count through the water bath without the interposed limb is used as baseline value. A reduction in the photon count below this baseline is assumed to be due to the bone. Muscles of the forearm have attenuation effect similar to that of water. The effects of varying muscle mass are thus eliminated by the water bath.

Degree of confidence:

Although SPA was widely used and although provide valuable a research data, the radionuclide source is a disadvantage. The energy source is subject to decay and must be replaced regularly. The low photon flux can cause the scanning time to be long (up to 40min), and spatial resolution tends to be poor. SPA machines repeatedly scanned in a single line and were limited (because of the physics of their operating principle) to measuring bone sites that could be either immersed in water or embedded in material with adsorption properties equivalent to soft tissue (to stimulate homogenous overlying soft tissue)

False positives / Negatives:

The precision error (coefficient of variation) is 1% for SPA. The precision error is affected not only by the measurement of technique but also subject characteristics. Precision error tends to increase in an elderly or osteoporotic population due to factors such as greater difficulty in repositioning and lower mean BMD.148

 

DPA (Dual Photon Absorptiometry) study               

DPA is an extension of the SPA principle that was developed to compensate for errors in SPA bone-mass measurement due to varying composition and thickness of surrounding soft tissues. This deficiency of SPA was over come by using 2 distinct photon energies, usually gadolinium153. Photons of different energy are differentially attenuated by bone and soft tissue. Therefore, their absorption by bone, and hence bone density, can be calculated by measuring the percentage of each transmitted beam and then by applying simple simultaneous equations. The source of photons is 153Ga, which emits photons of 2 discrete energies (44 and 100 keV). The scanning approach is similar to that of SPA.

 

Degree of confidence:

DPA represents an improvement over SPA in that it allows the direct measurement vertebral or femoral bone density. DPA eliminates the need for a constant soft tissue thickness across the scanning path (allowing its use in areas such as the spine and femur). DPA can be used to quantify changes in patient’s with metabolic bone disease or in those undergoing treatment with drugs that alter bone mineral content.

The desirable characteristics of DPA include its capability in assessing vertebral, proximal femoral or total body bone content; its independence from effect of marrow fat and other soft tissue, and its relatively low radiation dose. However, it is more expensive than other techniques, it has a lower scanning time, and it is not as widely available as SPA.

False Positive/ Negative:

With DPA, the error of precision and accuracy is 2-3%. One unavoidable source of error in the dual-photon technique is the fat distribution in the path of the radiation beam. It is possible to correct for an evenly distributed fat layer across the scanning path, but an uneven distribution introduces error in to the measurements.149

Ultrasound Measurement of Bone Density:                   

Finding: In 1984, Langton first described the measurement of broadband ultrasound attenuation (BUA) in the calcaneous as a potential indicator of hip fracture risk. The concept is based on the knowledge that the speed of sound and attenuation of sound wave are affected by density, compressibility, viscosity, elasticity, and structure of the material it is traveling though. This technique marked a departure from the conventional methods of bone density that used ionizing radiation. Ionizing radiation is attenuated at atomic level, whereas ultrasound is attenuated at the macroscopic structural level.  Some therefore, suggest that broadband ultrasound attenuation (BUA) depend on the macroscopic structure of cancellous bone in addition to the BMD assessed by using the ionizing radiation techniques.

BUA measurement in the calcaneus requires 1 transducer with 2 broadband ultrasound transducer components: one acts as a transmitter, and other acts as receiver. For a given material, ultrasound attenuation in always the same; this is known as the BUA index. To determine the attenuation index of any material (including bone) a broadband ultrasound frequencies is passed through the full thickness of material. The amplitude spectrums of the received signal in then compared with the spectrum of a reference material (water). By recording the frequency spectrum through water with and without the heel in position, a plot of attenuation with frequency is achieved. The difference between the 2 spectra is then plotted against frequency, giving a straight-line graph, the slope of which is the BUA index (in decibels per megahertz). The ultrasound frequencies used in the range of 0.1-1MHz. This range has become known as BUA.

Degree of confidence: QUS for bone analysis is a non-ionizing method in which the calcaneus as the measurement site. This technique is both a cost effective and accurate for identifying patients at risk of osteoporotic fracture. QUS has been scientifically validated in both fundamental in vitro studies and clinical in vivo studies. Clinical studies have shown that QUS parameters are sensitive to age related changes; they may be useful in distinguishing osteoporotic subject, and they offer a prospective prediction of fracture risk comparable to that of axial DEXA.

False positives/ Negatives: A number of factors can affect the accuracy and precision of BUA and produce false-positive or false-negative results. The anatomically incorrect placement of the region to be examined is 1 of these factors. Other factors are patient’s specific and may affect bone measurements; these are variability in bone width and soft tissue thickness or composition, marrow composition, and temperature. Error in measurement can be introduced by diffraction, which affect both attenuation and velocity measurements and is device specific.

 

DEXA (Dual Energy X-ray Absorptiometry):

DEXA is the method of choice to measure bone mineral density in elderly patient’s and others at risk of osteoporosis. Early detection is an important because fractures represent an enormous health burden. Central bone mineral density (BMD) measurement using DEXA is currently the gold standard for the diagnosis of osteoporosis.150 DEXA measurement can be completed by in about 15 to 20 minutes with minimal radiation exposure (about one tenth that of a standard chest X-ray).

Peripheral DEXA scans are inexpensive and are useful in screening large populations such as at health fair. The peripheral DEXA device is simple to operate. However, the sensitivity of peripheral DEXA for detecting osteoporosis is lower than that of central DEXA. Moreover, issues such as a lack of consensus on how results from peripheral sites are interpreted, poor correlation among the different machines, and precision errors prohibiting monitoring the patient’s who are receiving osteoporosis therapy limit the clinical utility of this technology.

Indication for obtaining a DEXA scan

Menopausal women should be evaluated clinically for osteoporosis risk in order to determine the need for BMD testing. All woman aged 65 or older, younger postmenopausal women with risk factors, and men aged 70 or older should undergo bone density testing. Risk factors include dementia, poor health, recent falls, prolonged immobilization, smoking, alcohol abuse, low body weight (<127 lb), history of fragility fracture in a first degree relative, estrogen deficiency at an early age (<45 years), and steroid use for more than 3 months.151

Adult who have a history of fragility fractures, have diseases associated with bone loss, or take medication that causes bone loss should also have DEXA scans.152 DEXA scans are also appropriate for monitoring a patient’s response to osteoporosis therapy.151

Site of measurement of BMD

The International Society for Clinical Densitometry recommends obtaining BMD measurements of the posteroanterior spine and hip. The lateral spine and ward’s triangle region of the hip should not be used for diagnosis, because these sites overestimate osteoporosis and results can be false positive. T-scores represent the standard deviations (SDs) comparing a patient’s BMD to that of a young adult (control), whereas Z-scores compare a patient’s, BMD to that of age matched controls. The World Health Organization (WHO) defines osteoporosis as T-score of 2.5 or below is either the spine or the hip.40

In the spine, the BMD of L1 through L4 should be reported unless there are vertebrae affected by severe degenerative changes or compression fractures. These should be excluded from the analysis because they falsely increased BMD. Most DEXA devices measure and report BMD of the total hip, femoral neck, and trochanter. The diagnostic classification of a patient is based on the lowest T-score of any of these hip sites.

Evidence suggest that the femur is the optimum site for predicting the risk of hip fracture153 and the spine is the optimum site for monitoring response to treatment.154 In very obese patient’s, those with primary hyperparathyroidism, or those in whom the hip or the spine, or both, can not be measured or interpreted, BMD may be measured in the forearm, using a 33% radius on the nondominant forearm.151

Interpretation of DEXA scans:   

Primary care physicians are usually not directly involved in the performance and interpretation of DEXA scans but should be familiar with the information on DEXA scan reports and how it applies to patient’s management.155 T-scores are used to diagnose osteoporosis, and Z-scores give the physician a sense of the age-appropriateness of bone loss. A Z-score of 2.0 or lower suggests a secondary cause and should trigger the search for underlying causes.156 In our practice, patient’s with a Z-scores below 1.0 are frequently found to have secondary causes, and such a score initiates a comprehensive search for these causes.

Although, postmenopausal osteoporosis is clearly the most common bone disease, secondary causes of osteoporosis are also quite common. Physicians need to actively look for these causes, either by thorough history taking or with biochemical studies.

Initiation of treatment:

Evidence showing an unacceptably high risk of fracture with T-scores of 2.5 and below and a significant reduction in fracture risk with treatment has made this threshold the initial criterion for the diagnosis of osteoporosis.155,156 However, the National Osteoporosis Foundation recommends initiating treatment to reduce fracture risk in women with T-scores below 2.0, even in the absence of risk factors, and in women with T-scores below 1.5 in the presence of one or more risk factors.157 Regardless of the T-score, patient’s with previous vertebral or hip fracture are classified as severely osteoporotic and should be treated. Recently the National Osteoporosis Risk Assessment study found osteoporotic fractures among patient’s who were classified as oeteopenic on the basis of the WHO criteria. There is now a move toward establishing a global fracture risk score that includes risk factors and BMD as a possible basis for initiating therapy.158

Monitoring response to treatment:

DEXA scans are useful in determining response to osteoporosis therapy. Under ideal conditions, the same technologist should perform DEXA scans on the same densitometer and under similar circumstances.

It is important to note that antiresorptive drug therapy leads to significant reduction of fracture risk, which can be obtained with very little improvement in BMD. Moreover, in interpreting serial DEXA scans, the actual BMD (in gm/cm2) should be compared and not the T-scores.

BMD remain the best and most useful marker for fracture risk reduction in clinical practice. The interval between BMD testing should be determined according to each patient’s clinical status. BMD measurements to monitor response to osteoporosis therapy should generally be obtained every year until stability is established, then at longer intervals, such as every 2 years.151 The posteroanterior lumbar spine is the optimum site to monitor therapy, and significant changes may be seen in a year or more, depending on the therapy used.154 Medicare permits physicians to repeat DEXA scans every 2 years157 or, in patient’s who are being monitored while on therapy, every year.

Osteoporosis in men:

The focus of osteoporosis management has been on postmenopausal women. However, osteoporosis in men is not rare.159 The estimated lifetime risk of fracture ranges from 13% to 25%.160 The three major causes of osteoporosis in men are alcohol abuse, glucocorticoid excess (from either endogenous Cushing’s syndrome or long-term glucocorticoid therapy), and hypogonadism.160,161 Bone density testing should be considered in men with fragility fractures; those taking drugs that may cause bone loss, such as androgen deprivation therapy for prostate cancer162; and men with multiple risk factors.

The International Society for Clinical Densitometry recommends that in men aged 65 years or older, osteoporosis should be diagnosed if T-scores are at or below 2.5. Between age 50 and 65years, osteoporosis should diagnosed if T-score are at or below 2.5 and other risk factors for facture are identified. In men under the age 50 years, diagnosis of osteoporosis should not be made on the basis of T-scores. Osteoporosis may be diagnosed clinically in men at any age with secondary causes of low BMD supported by the finding of low BMD.

It is important to know that the WHO classification, with its associated implications for fracture risk, was derived from a database composed purely of postmenopausal white women. Most densitometry devices now use the third National Health and Nutrition Examination Survey (NHANES III) database, which provide appropriate sex-matched controls for hip BMD.

Artifacts:

Certain conditions can artificially elevate the BMD, obscuring osteoporosis and leading to underestimation of fracture risk.163 These include degenerative changes seen in osteoarthritis and ankylosing spondylitis, structural abnormalities such as compression fracture164 and scolosis,165 aortic calcification, high-density objects on clothing, surgical implants,164 laminectomy,165 and retained radiopaque contrast agents.164 Vertebrae  with abnormal conditions should be excluded from the spine analysis. Similarly, BMD at the proximal femur can be altered by degenerative arthritis, degree of internal rotation, placement of soft tissue gluteal silicon implants,166 and overlying soft tissue thickness or fat.167 Patient’s positioning and appropriate placement of region of interest are paramount for precision and reproducibility.165 Physician should visually assess DEXA scans for artifacts that could affect BMD values. Going down the spine, the vertebrae become larger and have grater BMD (L1<L2<L3), and T-scores of individual vertebrae should be within approximately 1SD of each other. This observation does not apply to the hip, where differences greater than 1SD between regions may occurs because of different rates of loss cancellous and cortical bone from different hip sites.155

Automated analysis of spine scans in enhanced with the introduction of computer-aided densitometry, a software feature that assists physicians in the indentification of concealed osteoporosis or osteopenia in spine scans adversely affected by conditions that cause an artificial elevation in BMD.

Material and Methods:

The study was conducted in the Department of Medicine, Rajshahi Medical College Hospital from October 2005 to July 2006. 30(thirty) male and 30(thirty) female (total 60) patient’s were studied whose ages were >45years, H/O menopause >2years, low back pain, no pathological fracture of bone. Detailed history was taken from the patient’s. They were examined physically and requisite investigations were done. Their age, sex, occupation, height, weight, and special attention was given to the back pain, morning stiffness for at least 1 hour, heat intolerance, appetite, and alteration of bowel habit.

They were also asked about past history and drug history specially prednisolone, personal history specially smoking, family history especially non traumatic fracture of bone of their mother, any history of hypertension, diabetes mellitus.

During physical examination, along with examination of the locomotor system, general physical examination and a brief examination of all other systems also were done.

Plain X-ray of the lumbar spines and hip were done in all patient’s, using DEXA Bone Densitometer (XR36, Norland, USA), the spines and proximal femurs were studied in all patient’s. The results were then compared with the reference population data for individuals of the same age, sex, and ethnic background. The comparison was verified by age matched (Z-score) and Young reference (T-score). The interpretation was done by computer generated soft ware program following WHO recommendation (Table-4).

Table: 4 World Health Organization Definitions of osteoporosis based on Bone Density levels.

Normal Bone density within 1SD (+1SD or – 1SD) the young adult mean.
Low Bone mass (Osteopenia) Bone density within 1 to 2.5 SD (-1SD or – 2.5SD) below the young adult mean.
Osteoporosis Bone density 2.5 SD or more (> – 2.5 SD) below the young adult mean.
Severe Osteoporosis Bone density more than 2.5 SD below the young adult mean and there have been one or more osteoporotic fractures.

Completed blood count was done in all patient’s, other investigation like serum calcium level, urinary calcium level, serum albumin, X-ray skull, urinary benze Jones protein, and other necessary investigations were done in relevant cases to exclude secondary causes of osteoporosis.

Results:

Among the 60 cases, the mean age incidence was 58years, the youngest patient was 45 years and the oldest patient was 81 years. The maximum of cases were found in their 7th decades. The result is shown in Table-5.

In male patient’s, the maximum number of patient’s was in age group 60 & up years and also in female patient’s, the maximum number of patient’s, was in age group 60 & above years. This is shown in Table-6.

Among the 60 cases, the mean height incidence was 163.1 cm. The maximum number of cases was found in height group (cm) 160-169. This is shown in Table-7.

In male group, maximum number of patient’s, was in height group (cm) 160 –169; also in female group, the maximum number of patient’s was in height group (cm) 160 –169. This is shown in Table-8.

Among the 60 cases, the mean weight was 51.2 kg, the lowest weight was 30 kg, and the highest weight was 87 kg. The maximum number of cases was found in <50kg group. This is shown in the Table-9.

In male patient’s group, the maximum number of patient’s was in weight group <50 kg & also, the maximum number of patient’s, in female group, was in weight group <50 Kg. This is shown in Table-10.

Among 60cases, the mean Body mass Index (BMI) was 19.7kg/m2 The highest BMI was 33.1kg/m2 and the lowest BMI was 13 kg/m2. The maximum number of cases was found in BMI group<18.5 kg/m2. This is shown in Table-11.

In male group, the maximum number of patient’s were in BMI group 18.5 – 24.9, where as in female group, the maximum of patient’s were in BMI group <18.5. This is shown in Table-12.

Among 60 cases, 16 cases from urban and 44 cases from rural. This is shown in Table-13.

Both male and female patient’s were maximum from rural group. This is shown in Table-14.

Among 60 cases, incidence of bone mineral losses, was maximum in poor socioeconomic condition. This is shown in Table-15.

Maximum incidence of bone mineral losses among male and female groups, were also in poor socioeconomic conditions. This is shown Table-16.

Among 30 female patient’s, all of their occupations were house, wife, but in male patient’s, the incidence was maximum in other’s occupation (like landlord). This is shown in Table-17.

Among 30 male patient’s, 23 (76.7%) were smoker & among 30 female patient’s, 1 (3.3%) were smoker.  This is shown in Table-18.

No male patient’s had history of non traumatic fracture of the bone of their mothers. But among female patient’s, only eight patients had history of non-traumatic fracture of bone of their mothers. This is shown in Table-19.

Among male patient’s, only 1 patient had diabetes mellitus, and among female patient’s only 1 patient had diabetes mellitus. This is shown in Table-20.

Among 30 female patient’s, maximum patient’s were in 5-10 years group of menopausal durations. This is shown in Table-21.

Among 60 patient’s, the maximum patient’s were in back pain duration >1year. This is shown in Table-22.

Among male patient’s, maximum 19 patients had back pain duration >1year and among female patients, maximum 16 patient’s had back pain duration < 1 year. This is shown in Table-23.

The bone mineral densities are shown in Table-24. Four patient’s (male-3; Female-1) were found to have normal bone density, whereas the rest 56 patient’s had shown different grades of bone mineral loss. Among the 56 patient’s, 17 patient’s (Male-10; Female-7) suffered from osteopenia. Fourteen patients (Male-4; Female-10) had shown osteoporosis in both femoral neck and lumbar vertebra. The rest 25 patient’s (Male-13; Female-12) had shown combined osteopenic & osteoporotic changes either in lumber vertebra and / or femur. This is shown in Table-25.

BMD was higher in all sites in male than female. Osteophytes, which were common in older people, may have influenced lumber spine BMD result. This is shown in Table-26.

Among 4 normal BMD presentation patient’s, 1(25%) was in 50-54 years group & 2 (50%) were in 55-59 years group & 1 (25%) was in 60 & up years group. Among 17 osteopenic BMD presentation patient’s, 8 (47%) were in 45-49 years group & 1 (5.9%) was in 50-54 years group & 3 (17.6%) in 55-59 years group & 5 (29.4%) in 60 & up years group. Among 14 osteoporotic BMD presentation patient’s, 1 (7.1%) in 55-54 years group, & 1 (7.1%) in 55-59 years group & 12 (85.7%) in 60 & up years group. Among 25 combined BMD presentation patient’s, 2 (8%) in 45-49 years group & 5 (20%) in 50-54 years group & 6 (24%) in 50-59 years group & 12 (48%) in 60 and up years group. This is shown in Table-27.

Among 4 normal BMD presentation patient’s, 1 (25%) in 50-59 kg group & 3 (75%) in 60-69 kg group. Among 17 osteopenic BMD presentation patietns, 5 (29.4%) in < 50kg group & 4 (23.5%) in 50-59 kg group & 4 (23.5%) in 60-69kg group & 4 (23.5%) in 70 & up kg group. Among 14 osteoporotic BMD presentation patient’s, 11 (78.6%) in <50kg group & 3 (21.4%) in 50-59kg group & among 25 combined BMD presentation patient’s, 16 (64%) in<50kg group & 5 (20%) in 50-59 kg group & 3 (12%) in 60-69 kg group & 1 (4%) in 70 & up kg group. This is shown in Table-28.

Among 60 patient’s, 1 (25%) normal BMD presentation patient’s was in 150 –159 cm group & 3 (75%) were in 160 –169 cm group. 3 (17.6%) osteopenic BMD presentation patient’s are in height group 150-159 & 11(64.7%) osteopenic BMD presentation patient’s are in height group 160 –169 cm & 3 (17.6%) osteopenic BMD presentation patient’s are in height group 170 & up cm group. In osteoporotic BMD presentation patient’s, 1 (7.1%) are in height group <150cm, & 5(35.7%) are in height group 150-159 cm group, & 7 (50%) are in 160-169 cm & group, & 1 (7.1%) are in height group 170 & up cm. In Combined BMD presentation patient’s group, 5 (20%) are in height group 150-159cm, and 16 (64%) are in height group 160-169 cm, & 4 (16%) are in height group 170 & up cm. This is shown in Table-29.

In normal BMD presentation patient’s, 2 (50%) have BMI in 18.5-24.9 kg / m2  group, & 2 (50%) have BMI in 25-29.9 kg/m2 group. In osteopenic BMD presentation patient’s 3 (17.6%) patient’s BMI in < 18.5kg/m2 group, and 10 (58.8%) in 18.5-24.9kg/m2 BMI group, & 2 (11.8%) in 25-29.9 kg/m2 BMI group & 2 (11.8%) in 30 & up kg/m2 BMI group. In osteoporotic BMD patient’s, 11(78.1%) in < 18.5kg/m2 BMI group & 3 (21.4%) in 18.5-24.9kg/m2 BMI group. In combined BMD presentation patient’s, 13 (52%) in < 18.5kg/m2 BMI group & 11 (44%) in 18.5 –24.9kg/m2 BMI group & 1 (4%) in 25-29.9kg/m2 BMI group. This is shown in Table-30.

In normal BMD presentation patient’s, 1 (25%) are poor & 3 (75%) are in middle class. In osteopenic BMD presentation patient’s, 10 (58.8%) are poor & 6 (35.3%) are in middle class & 1 (5.9%) are in rich group. In osteoporotic BMD presentation patient’s, 8 (57.2%) are poor & 5 (35.7%) are in middle class & 1 (7.2%) are in rich group. In combined BMD presentation patient’s, 14 (56%) are poor & 11 (44%) are middle class. This is shown in Table-31.

Among 30 female patient’s, all were housewives. Among 30 male patient’s, in normal BMD presentation patient’s, 1 (33.3%) patient’s occupation was service & 2 (66.7%) patient’s occupation were others. In osteopenic BMD presentation male patient’s 1(10%) patient occupation was labor & also same number patient occupation, is business & 8 (80%) patient’s occupation were others. In osteoporotic BMD presentation male patient’s, 2 (50%) patient’s occupation were business & also same number of patient’s occupations was other. In combined BMD presentation male patient’s, 2 (15.4%) patient’s occupation were labor & also same number of patient’s occupation were service, business & 7 (53.8%) patient’s occupation were others. This is shown in Table-32.

Among 60 patient’s, in normal BMD presentation patient’s, 2 (50%) patient’s were in urban & 2 (50%) patient’s were in rural. In osteopenic BMD presentation patient’s, 4 (23.5%) were in urban & 13 (76.5%) patient’s were in rural. In osteoporotic BMD presentation patient’s, 3 (21.4%) patient’s were in urban & 11 (78.6%) patient’s were in rural. In combined BMD presentation patient’s, 7(28%) patient’s were in urban & 18 (72%) patient’s were in rural. This is shown in Table-33.

In normal BMD presentation patient’s, 2(50%) have smoking history. In osteopenic BMD presentation patient’s, 8 (47%) have smoking history. In osteoporotic BMD presentation patient’s, 4 (28.6%) have smoking history. In combined BMD presentation patient’s, 10(40%) have smoking history. This is shown Table-34.

Among 30 male patient’s, none of them have family history (non traumatic fracture of the bone of their mother). But among 30 female patient’s, in osteopenic BMD presenting female patient’s, 2 (28.6%) patient’s have family history positive. In osteoporotic BMD presenting female patient’s, 1 (10%) have family history positive. In combined BMD presenting female patient’s, 5 (41.7%) patient’s have family history positive. This is shown in Table-35.

Among the 60 patient’s, 2 patient’s were diabetic. In the normal BMD presetting patient’s 01 (25%) patient is diabetic, which is 25%, and in combined BMD presenting patient’s, 1(4%) patient is diabetic. So, incidence of diabetics with normal BMD presenting patient’s is higher. This is shown in Table-36.

Among the 30 female patient’s, normal BMD presenting patient’s, 1 (100%) patient menopause duration was 5-10years group. In osteopenic BMD presenting female patient’s, 4 (57.1%) patient’s menopausal duration was < 5years group and 2 (28.6%) patient’s menopausal duration was 5-10years group and 1(14.3%) patient’s menopausal duration was 10 & up years group in osteoporotic BMD presenting female patient’s, 3 (30%) patient’s menopausal duration was 5-0 years group, and 7 (70%) patient’s menopausal duration was 10 & up years group. In combined BMD presenting female patient’s, 2 (16.7%) patient’s menopausal duration was <5years group & 7 (58.3%) patient’s menopausal duration was 5-10 years group, & 3 (25%) patient’s menopausal durations was 10 & up years group. This is shown in Table-37.

In normal BMD presenting patient’s, 2 (50%) patient’s back pain duration was <1 year group, & 2 (50%) patient’s back pain duration was >1 year group. In osteopenic BMD presenting patient’s, 9(52.9%) patient’s back pain duration was <1year group, & 8 (47%) patient’s back pain duration was >1year. In osteoporotic BMD presenting patient’s, 6(42.8%) patient’s back pain duration was <1year group, & 8(57.2%) patient’s back pain duration was> 1year group. In Combined BMD presenting patient’s, 10(40%) patient’s back pain duration was < 1year group, & 15 (60%) patient’s back pain duration was > 1year group. This is shown in Table-38.

In normal BMD presenting patient’s, 25% have systolic blood pressure was < 140mm of Hg and 75% patient’s blood pressure were in 140-160 mm of Hg group. In osteopenic BMD presenting patient’s, 52.9% patient’s have systolic B.P. <140 mm of Hg group and 47.1% patient’s have systolic B.P. in 140-160 mm of Hg group. In osteoporotic BMD presenting patient’s, 57.1% paitents have systolic B.P.  was < 140 mm of Hg group and 42.9% patient’s have systolic B.P was 140 –160 mm of Hg group. In combined BMD presenting patient’s, 48% patient’s systolic B.P. equally was in < 140 mm of Hg and 140 – 160 mm of Hg group and 4% patient’s systolic B.P. was in > 160mm of Hg group. This is shown in Table-39.

In normal BMD presenting patient’s, 25% patient’s diastolic B.P. was in <90mm of Hg & 75% patient’s diastolic B.P was in 90-100 mm of Hg group. In osteopenic BMD presenting patient’s, 82.4% patient’s diastolic B.P. was in <90mm of Hg & 17.6% patient’s diastolic B.P was in 90-100 mm of Hg group. In osteoporotic BMD presenting patient’s, 71.4% patient’s diastolic was < 90 mm of Hg group & 28.6% patient’s diastolic B.P was in 90-100 mm of Hg group. In combined BMD presenting patient’s, 76% patient’s diastolic B.P was in < 90mm of Hg group & 24% patient’s diastolic BP was in 90-100 mm of Hg group. This is shown in Table-40.

Among the male patient’s, 24(80%) patient’s have degenerative changes and 4(13.3%) patient’s have osteoporotic changes and 2 (6.7%) patient’s have normal finding on X-ray L-S spine. In female patient’s, 3 (10%) have normal finding and 9(30%) patient’s have osteoporotic changes & 10 (30.3%) patient’s have degenerative changes and 8 (26.7%) patient’s have combined changes on X-ray L-S spine. This is shown in Table-41.

Sensitivity of the X-ray in assessing BMD is 39%. This is shown in Table-42.

Table- 5

Age incidence

Total patient’s = 60

Age group (years)

Number of Patient’s

Percentage

45 – 49

10

16.7%

50 – 54

8

13.3%

55 – 59

12

20%

60 & up

30

50%

Table-6

Age incidence between male & female group

Age group (years)

45 – 49

50 – 54

55 – 59

60 & up

No of pt

%

No of pt

%

No of pt

%

No of pt

%

Male       No =30

6

20

4

13.3

2

6.7

18

60

Female No= 30

4

13.3

4

13.3

10

33.3

12

40

Table-7

Height incidence

Total patient’s=60

Height group (cm)

Number of Patient’s

Percentage

< 150

1

1.7%

150 – 159

14

23%

160 – 169

37

61%

 170 & up

8

13%

Table-8

Height incidence between male & female group

Height group (cm)

< 150

150 – 159

160 – 169

170 & up

No of pt

%

No of pt

%

No of pt

%

No of pt

%

Male       No =30

5

16.7

17

56.7

8

26.7

Female No= 30

1

3.3

9

30

20

66.7

Table-9

Weight incidence

Total patient’s=60

Weight group (kg)

Number of Patient’s

Percentage

< 50

32

53.3%

50 – 59

13

21.7%

60 –69

10

16.7%

 70 & up

5

8.3%

Table-10

Weight incidence between male & female group

Weight group (kg)

< 50

50 – 59

60 – 69

70 & up

No of pt

%

No of pt

%

No of pt

%

No of pt

%

Male       No =30

13

43.3

8

26.7

6

20

3

10

Female No= 30

19

63.3

5

16.7

4

13.3

2

6.7

Table-11

BMI incidence

Total patient’s=60

BMI group (kg/m2)

Number of Patient’s

Percentage

< 18.5

27

45%

18.5 – 24.9

26

43.3%

25 –29.9

5

8.3%

30 & up

2

3.3%

Table-12

BMI incidence between male & female group

BMI group (kg/m2)

<18.5

18.5 – 24.9

25 –29.9

30 & up

No of pt

%

No of pt

%

No of pt

%

No of pt

%

Male       No =30

12

40

13

43.3

4

13.3

1

3.3

Female No= 30

15

50

13

43.3

1

3.3

1

3.3

Table-13

Address incidence

Total patient’s 60

Address

Number of Patient’s

Percentage

Urban

16

26.7%

Rural

44

73.3%

Table-14

Address incidence between male & female group

Address

Urban

Rural

No of pt

%

No of pt

%

Male       No =30

5

16.7

25

83.3

Female No= 30

11

36.7

19

63.3

Table-15

Incidence in different socioeconomic condition

Total patient’s=60

Socioeconomic condition

Number of Patient’s

Percentage

Poor

33

55%

Middle Class

25

41.7%

Rich

2

3.3%

Table-16

Socioeconomic incidence between male & female group

Socioeconomic condition

Poor

Middle Class

Rich

No of pt

%

No of pt

%

No of pt

%

Male       No =30

17

56.7

12

40

1

3.3

Female No= 30

16

53.3

13

43.3

1

3..3

Table-17

Occupational Status in male patient’s

 

Occupation

Number of patient’s (No =30)

Percentage (%)

Labor

3

10%

Service

3

10%

Business

5

16.7%

Others

19

63.3%

 

Table-18

Smoking incidence in different sexes

Patient’s

Number of patient’s

Percentage (%)

Male               No = 30

23

76.7%

Female          No = 30

1

3.3%

Table-19

Family history incidence

Patient’s

Family history positive

Percentage (%)

Female          No = 30

8

26.7

Table-20

Patient’s

Diabetic history

Percentage (%)

Male               No = 30

1

3.3%

Female          No = 30

1

3.3%

Table-21

Menopausal duration incidence

Menopausal duration (Years)

Number of Patient’s

Percentage

<5

6

20%

5 – 10

13

43.3%

10 & up

11

36.7%

Table-22

Back pain duration incidence

Back pain duration (Years)

Number of Patient’s

Percentage (%)

< 1

27

45%

> 1

33

55%

Table-23

Back pain duration incidence in different sexes

Back pain duration (Years)

< 1

> 1

No of pt

%

No of pt

%

Male       No =30

11

36.7

19

63.3

Female No= 30

16

53.3

14

46.7

Table-24

Bone mineral density (in gm/cm2) of lumbar vertebrae

and femoral neck in different categories.

Normal

No = 4

Osteopenia

No = 17

Osteoporosis

No = 14

Combined                    No = 25

Osteopenia

Osteoporosis

Site

LV

FN

LV

FN

LV

FN

LV

FN

LV

FN

BMD (SD)

1.2000

.05

1.0128

.02

.8396

.03

.7731

.06

.5860

.04

.5976

.03

.8250

.03

.8170

.01

.5484

0

.6502

.03

T-Score

(SD)

.73

.07

.48

.01

1.56

.02

1.88

.05

3.19

.01

3.52

.01

1.73

.01

2.05

.02

3.42

0

3.26

.09

* LV = lumbar vertebrae; FN= Femoral Neck; * Combined= Osteoporosis + osteopenia.

Table-25

Bone Mineral losses in different sexes.

Patient’s

Normal

No = 4

Osteopenia

No = 17

Osteoporosis

No = 14

Combined

No = 25

No of pt

%

No of pt

%

No of pt

%

No of pt

%

Male       No=30

3

10

10

33.3

4

13.3

13

43.3

Female No=30

1

3.3

7

23.3

10

33

12

40


Table-26

Comparison of male (M) and female (F) population for lumbar spine and femoral neck bone mineral densities stratified by age groups.

Age (years)

No

Spine (gm/cm2)

[mean SD]

Femur (gm/cm2) [mean SD]

45 – 49

M (6)

.9043 .09

.8432  .08

F (4)

.8850  .14

.7654  .07

50 – 54

M (4)

.9840 .16

.9147  .12

F (5)

.7497  .18

.6602  .07

55 – 59

M (2)

.9076 .004

.7697  .01

F (9)

.7912  .21

.6984  .01

60  & up

M (18)

.8470 .19

.7440  .16

F (12)

.6387  .15

.5737  .08

Table-27

Association with age

Presentation

45 – 49 years

50 – 54 years

55 – 59 years

60 & up years

No of pt

%

No of pt

%

No of pt

%

No of pt

%

Normal           No=4

1

25

2

50

1

25

Osteopenia     No=17

8

47

1

5.9

3

17.6

5

29.4

Osteoporosis  No=14

1

7.1

1

7.1

12

85.7

Combined       No=25

2

8

5

20

6

24

12

48

Table-28

Association with weight

Presentation

< 50 kg

50 – 59 kg

60 – 69 kg

70 & up kg

No of pt

%

No of pt

%

No of pt

%

No of pt

%

Normal           No=4

1

25

3

75

Osteopenia     No=17

5

29.4

4

23.5

4

23.5

4

23.5

Osteoporosis  No=14

11

78.6

3

21.4

Combined       No=25

16

64

5

20

3

12

1

4


Table-29

Association with Height

Presentation

< 150 cm 

150 – 159cm

160 – 169 cm

170 & up cm

No of pt

%

No of pt

%

No of pt

%

No of pt

%

Normal           No=4

1

25

3

75

Osteopenia     No=17

3

17.6

11

64.7

3

17.6

Osteoporosis  No=14

1

7.1

5

35.7

7

50

1

7.1

Combined       No=25

5

20

16

64

4

16

Table-30

Association with BMI

Presentation

< 18.5 kg/m2 

18.5 – 24.9 kg/m2

25 – 29.9 kg/m2

30 & up kg/m2

No of pt

%

No of pt

%

No of pt

%

No of pt

%

Normal           No=4

2

50

2

50

Osteopenia     No=17

3

17.6

10

58.8

2

11.8

2

11.8

Osteoporosis  No=14

11

78.6

3

21.4

Combined       No=25

13

52

11

44

1

4

Table-31

Association with Socioeconomic condition

Presentation

Poor

Middle Class

Rich

No of pt

%

No of pt

%

No of pt

%

Normal           No=4

1

25

3

75

Osteopenia     No=17

10

58.8

6

35.3

1

5.9

Osteoporosis  No=14

8

57.2

5

35.7

1

7.2

Combined       No=25

14

56

11

44

Table-32

Association with Occupation

Presentation

Labor

Service

Business

Others

No of pt

%

No of pt

%

No of pt

%

No of pt

%

Normal           No=3

1

33.3

2

66.7

Osteopenia     No=10

1

10

1

10

8

80

Osteoporosis  No=4

2

50

2

50

Combined       No=13

2

15.4

2

15.4

2

15.4

7

53.8

Table-33

Association with address

Presentation

Urban

Rural

No of pt

%

No of pt

%

Normal             No=4

2

50

2

50

Osteopenia        No=17

4

23.5

13

76.5

Osteoporosis     No=14

3

21.4

11

78.6

Combined         No=25

7

28

18

72

Table-34

Association with Smoking

Presentation

No of pt

%

Normal             No=4

2

50

Osteopenia        No=17

8

47

Osteoporosis     No=14

4

28.6

Combined         No=25

10

40

Table-35

Association with Family history

Presentation

No of pt

%

Normal             No= 1

Osteopenia        No= 7

2

28.6

Osteoporosis     No= 10

1

10

Combined         No= 12

5

41.7

Table-36

Association with D.M.

Presentation

No of pt

%

Normal             No= 4

1

25

Osteopenia        No= 17

0

0

Osteoporosis     No= 14

0

0

Combined         No= 25

1

4

 

Table-37

Association with duration of menopause

Presentation

< 5 years 

 5 – 10 years 

10 & up years

No of pt

%

No of pt

%

No of pt

%

Normal           No=1

1

100

Osteopenia     No=7

4

57.1

2

28.6

1

14.3

Osteoporosis  No= 10

3

30

7

70

Combined       No= 12

2

16.7

7

58.3

3

25

Table-38

Association with duration of back pain

Presentation

< 1 Year 

> 1 Year

No of pt

%

No of pt

%

Normal             No=4

2

50

2

50

Osteopenia        No=17

9

52.9

8

47

Osteoporosis     No=14

6

42.8

8

57.2

Combined         No=25

10

40

15

60

 

Table-39

Relation with systolic BP

Presentation

< 140  mm of Hg

140 – 160 mm of Hg

> 160  mm of Hg

No of pt

%

No of pt

%

No of pt

%

Normal           No=4

1

25

3

75

Osteopenia     No=17

9

52.9

8

47.1

Osteoporosis  No=14

8

57.1

6

42.9

Combined       No=25

12

48

12

48

1

4

Table-40

Relation with diastolic BP

Presentation

< 90  mm of Hg

90 – 100 mm of Hg

> 100  mm of Hg

No of pt

%

No of pt

%

No of pt

%

Normal           No=4

1

25

3

75

Osteopenia     No=17

14

82.4

3

17.6

Osteoporosis  No=14

10

71.4

4

28.6

Combined       No=25

19

76

6

24

Table-41

X- ray finding in different sexes.

Patient’s 

X-ray L-S spine

Normal

Osteoporotic changes

Degenerative changes

Combined (Both Osteo. + Degen. Changes)

No. of pt.

%

No. of pt.

%

No. of pt.

%

No. of pt.

%

Male        No =30

2

6.7

4

13.3

24

80

Female    No =30

3

10

9

30

10

33.3

8

26.7

 

Table-42

X-ray finding

Bone loss found in BMD

No bone loss found in BMD

Positive scan

20

1

Negative scan

31

8

51

9

Discussion:

The present study was under taken in elderly patient’s presenting with low back pain to evaluate the frequency of osteoporotic changes in skeleton and to evaluate the sensitivity of radiology for assessing bone density in medicine units of Rajshahi Medical College Hospital from 12-10-2005 to 16-07-2006. A total 60 cases were studied. Among them 30 patient’s were male & 30 patient’s were female. In this series, the peak incidence of bone mineral losses occurred in 60 & up year’s age group. Next age group was 55-59 years. 50% of patient’s in 60 & up year’s age group and 20% of patient were 55-59 years age group. In male patient’s, highest 60% were in 60 & up years age groups, 2nd highest 20% were in 45-49 years age group, In female patient’s, highest 40% were in 60 & up years age group, second highest 33.3% were in 55-59 years age group. The youngest patient was 45 years and oldest patient was 81 years. On the basis of many epidemiologic clinical and laboratory findings, Riggs and his colleagues have proposed that evolutional osteoporosis is divided in to two major and distinct syndromes, ie, Type- I : post menopausal osteoporosis & Type – II : Age related osteoporosis.168 This study is very much similar to the mentioned categories. 168

Mean height was 163.1cm. Maximum patient’s was in 160-169cm group. Next height number of patient’s was in 150-159 cm group. So 61% patient’s were in 160-169cm height group, & 23% patient’s were in 150-159cm height group. In male patient’s, highest 56.7% were in 160-169 cm height group and next 26.7% of patient’s were in 170 & up cm height group and patient’s in < 150cm height group. In female patient’s, highest 66.7% of patient’s also were in 160-169 cm height group and next 30% of patient’s were in 150-159cm height group and no patient in 170 and up cm height group.

Normal BMD presentation patient’s group, 75% were in 160-169 cm weight group and next 25% were in 150-159cm group. In osteopenic BMD presenting patient, highest 64.7% were in 160-169cm group & next highest 17.6% were in equally in 150-159 cm & 170 and up cm groups. In osteoporotic BMD presenting patient’s, highest 50% were in 160-169 cm group & next 35.7% were in 150-159cm group and 7.1% were equally in < 150 cm & 170 & up cm groups. In combined BMD presenting patient’s, highest 64% patient’s were in 160-169 cm group and next highest 20% were in 150-159cm group. So there is association between the height and bone mineral losses.118, 119

The maximum number patient’s was in < 50kg weight group. Next maximum number of patient’s was in 50-59kg weight group. So 53.3% were in <50kg group and 21.7% were in 50-59kg group. In male patient’s 43.3% were in <50kg group & next highest 26.7% were in 50-59kg group. In female patient’s, highest 63.3% were in <50kg group and next 16.7% were in 50-59 kg group. In normal BMD presenting patient’s, 75% were in 60-69kg group and next 25% were in 50-59kg group. In osteopenic BMD presenting patient’s maximum 29.4% were in <50kg group and next 23.5% were equally distributed to the rest of the groups. In osteoporotic BMD presenting patient’s, highest 78.6% were in <50kg group and in combined BMD presenting patient’s, highest64% were in <50kg group. So there is positive relationship between weight & bone mineral density.120, 127, 169.

The maximum of patient’s BMI were in < 18.5kg /m2 group & next highest number of patient’s were in 18.5 –24.9kg/m2 group. 45% were in < 18.5kg/m2 group and next highest 43.3% were in 18.5-24.9 kg /m2. In male patient’s, 43.3% group were in 18.5-24.9kg/m2 and next highest 40% were in <18.5 kg /m2 group. In Female patient’s, highest 50% were in <18.5kg/m2 group and next highest 43% were in 18.5-24.9 kg/m2 group. In normal BMD presenting patient’s, 50% equally in 18.5-24.9 kg/m2 and 25-29.9 kg/m2 groups. In osteopenic BMD presenting patient’s, maximum 58.8% were in 18.5-24.9 kg/m2 group and next highest 17.6% were in <18.5 kg/m2. In osteoporotic BMD presenting patient’s, maximum 78.6% were in < 18.5% kg/m2 group and next 21.4% were in 18.5-24.9 kg/m2 group. In combined BMD presenting patient’s, highest 52% were in <18.5 kg/m2 group & next highest 44% were in 18.5-24.9 kg/m2 group. So body mass index (BMI) has positive correlation with bone mineral density which is consistent with the study by C.A.F. Zerbini et all from Brazil (2000).170

Highest number of patient 44 (73.3%) from rural, and 16 (26.7%) from urban. In male patient 25(83.3%) from rural and in female patient’s 19(63.3%) from rural. In normal BMD presenting patient’s, 50% equally from urban & rural. In osteopenic BMD presenting patient’s, 76.5% from rural, & 23.5% from urban. In osteoporotic BMD presenting patient’s, 78.6% from rural & 21.4% from urban. In combined BMD presenting patient’s, 72% from rural & 28% from urban. So in rural population, bone mineral losses higher than urban population.

Highest number 33 (55%) patient’s are poor, and then 25(41.7%) patient’s are in middle class. In male patient’s, 56.7% patient’s are poor and then 40% patient’s are in middle class. In female patient’s, 53.3% patient’s are in poor & then 43.3% patient’s are in middle class. In normal BMD presenting patient’s, 75% patient’s are in middle class and 25% patient’s are in poor. In osteopenic BMD presenting patient’s, 58.8% are in poor and 35.3% patient’s are in middle class. In osteoporotic BMD presenting patient’s, highest 75.2% patient’s are poor and than 35.7% patient’s are in middle class. In combined BMD presenting patient’s, 56% are poor & then 44% patient’s are in middle class. So in poor socioeconomic condition, bone mineral losses is high, which in consistent with the study by May-Choowang, et all from USA (2006).171

All female patient’s occupation were housewife. But in male patient’s, others (like land lord) occupation were 63.3% & 16.7% patient’s occupation were business & 10% patient’s occupation equally were labor & service. In normal BMD presenting male patient’s, 66.7% patient’s occupation were others & 33.3% patient’s occupation were service. In osteopenic BMD presenting patient’s, 80% patient’s occupation were others and 10% patient’s occupation equally were business and labor. In osteoporotic BMD presenting male patient’s, 50% patient’s occupation were others and 50% patient occupation were business. In combined BMD presenting male patient’s, 53.8% patient’s occupation were other’s and 15.4% patient’s occupation equally were labor, service and business. So BMD losses marked in other’s occupation patient’s, in which occupation physical labor is minimal.32 So BMD has positive correlation with physical activity which is consistent with the study by Alex A. Florindo, et al from Brazil (2002)172

None of the male patient’s have family history positive. Among female patient’s, only 26.7% patient’s have family history of nontraumatic fractures of bones. In osteopenic BMD presenting patient’s, only 28.6% female patient’s family history positive. In osteoporotic BMD presenting female patient’s, only 10% patient’s have family history positive. In combined BMD patient’s 41.7% patient’s have family history positive. So, those who are family history positive, much of them in combined BMD that is either osteoporosis of lumber vertebra and osteopenia of femoral neck or osteoporosis femoral neck and osteopenia of lumber vertebra. This study consistent with the study by Eric S. Orwoll, et all in 1996.173

Among male patient’s, only 3.3% of patient’s have D.M. & among female patient’s, only 3.3% patient, have D.M. In normal BMD presenting patient’s, 25% patient’s have D.M. and in combined BMD presenting patient’s, only 4% patient’s have D.M. So there is no association between BMD & D.M. This study is consistent with the study by M. Sert, et all in 2003.174

Among the male patient’s, 76.7% patient’s are smokers and only among female patient’s, only 3.3% patient’s are smokers. In normal BMD presenting patient’s, 50% patient’s are smokers. In osteopenic BMD presenting patient’s, 47% patient’s are smokers. In osteoporotic BMD presenting patient’s, only 28.6% patient’s are smokers. In combined BMD presenting patient’s, 40% patient’s are smokers. So there is no significant relation between smoking and BMD. In 1994, H May, el al in U.K. also shown that there is no significant relation between smoking and BMD.175

Among female patient’s, 43.3% patient’s menopausal duration are 5-10 years group. Next highest 36.7% female patient’s menopausal duration are 10 and up years group. In normal BMD presenting patient’s, 100% are in 5-10 years group. In osteopenic BMD presenting patient’s, highest 57.1% patient’s are in <5years menopausal duration group and next 28.6% patient’s are in 5-10 years menopausal duration group. In osteoporotic BMD presenting patient’s, maximum 70% patient’s are in 10and up years menopausal duration group and next 30% patient’s are in 5-10 years menopausal duration group. In combined BMD presenting patient’s, 58.3% patient’s are in 5-10 years menopausal duration group and next maximum 25% patient’s are in 10 and up years menopausal duration group. So there is negative association beteen BMD and menopausal duration. S. Chowdhury, et al (2001) from Dhaka also got negative association between BMD and menopausal duration.169

45% patient’s back pain duration <1years group & 55% patient’s back pain duration> 1 year. In male patient’s, 63.3% patient’s back pain duration > 1years group and only 36.7% patient’s back pain duration <1year.  In female patient’s, 53.3% patient’s back pain duration < 1years group and 46.7% patient’s back pain duration are in > 1year group. In normal BMD presenting patient’s, 50% patient’s are equally distributed in both groups. In osteopenic BMD presenting patient’s, 52.9% patient’s are in <1year back pain group. In osteoporotic BMD presenting patient’s, 57.2% patient’s are in >1year back pain group. In combined BMD presenting patient’s, 60% patient’s are in > 1year back pain duration group. So there is an positive association between BMD and back pain duration. Takashi Manabe in 2003 have shown that there is positive relation between BMD and back pain.176

In normal BMD presenting patient’s, 25% patient’s have systolic B.P. <140mm of Hg and 75% patient’s have systolic B.P. 140-160 mm of Hg. group. In osteopenic BMD presenting patient’s, 52.9% patient’s have systolic B.P. < 140 mm of Hg and 47.1% patient’s have systolic B.P. in 140-160mm of Hg. In osteoporotic BMD presenting patient’s, 57.1% patient’s have systolic B.P. < 140mm of Hg group and 42.9% patient’s have systolic B.P. 140 –160 mm of Hg. In combined BMD presenting patient’s, 48% patient’s systolic equally in <140mm of Hg and 140-160mm of Hg. group and 40% patient’s have systolic B.P. in >160 mm of Hg. group. So there is no association between systolic B.P. and BMD.

In normal BMD presenting patient’s, 25% patient’s have diastolic B.P. <90mm of Hg and 75% patient’s have diastolic B.P. in 90-100 mm of Hg. group. In osteopenic BMD presenting patient’s, 82.4% patient’s have diastolic B.P. < 90 mm of Hg and 17.6% patient’s have diastolic B.P. in 90-100mm of Hg. In osteoporotic BMD presenting patient’s, 48% have diastolic B.P. equally distributed in < 90mm of Hg and 90-100 mm of Hg groups and 4% patient’s have diastolic B.P. >160 mm of Hg groups. So there is no association between diastolic B.P. and BMD.  But E. A. Jan Kowska, et al in 2002 have shown that there is no relationship between BMD and systolic B.P., but inverse relationship between BMD and diastolic B.P.177

In the present study BMD at the lumbar spine and femoral neck level was higher for men than for women in all age groups. BMD at the femoral neck level deceased for both sexes with age but reduction was lesser and later for men. BMD is higher in lumber vertebra then for femoral neck, this is because of osteophytes. This study is consistent with the study by C. A. F. Zerbini, et all from Brazil (2002).170 Radiology is of limited value unless there is severe bone loss or compression fracture occur. Radiology is the least sensitive method for assessing for bone density. This study is consistent with the study by selim M Ansari, et all from Bangladesh (2002).178


Summary and Conclusion: 

A series of 60 cases were studied which included 30 male & 30 female elderly patient’s presenting with low back pain in medicine units of Rajshahi Medical College Hospital, Rajshahi. The mean age of the patient was 58 years. Maximum number of patient’s height is 160-169cm group. Maximum number of patient’s weight were <50kg (male>female) in weight. 50%female & 40% male patient’s BMI were <18.5kg /m2. About 73.3% patient’s were from rural origin. Maximum patient’s were poor. About 76.7% male patient’s were smoker. Females were housewives and most male patient’s occupation were different. Only 26.7% female patient’s had family history of nontraumatic fracture of bones of their mothers. Most of the female patient’s menopausal duration was >5 years.  Maximum female patient’s back pain duration was <1year and maximum male patient’s back pain duration was >1year. Maximum male patient’s presented as either osteopenic of combined BMD and maximum female patient’s either osteoporotic or combined (osteoporosis of the lumber vertebra and osteopenia of the femoral neck or osteoporosis of the femoral neck and osteopenia of the lumber vertebra). There was an inverse relationship between BMD and the age. There was an positive relationship between weight and BMD. Body mass index (BMI) had positive relation with the BMD. Bone mineral losses were high in poor socioeconomic condition. In male patient’s BMD losses marked in other’s type occupation, in which physical labor was minimal. Bone mineral losses were higher in rural population than urban population. Those who had family history that is history of nontraumatic fracture of bones of their mothers, many of them had combined reduction of BMD (either osteoporosis of the lumber vertebra and osteopenia and femoral neck or osteopenia of the lumber vertebra and osteoporosis of the femoral neck) and also reduced BMD. There was no significant relation between smoking and BMD. There was also no relationship between D.M. and BMD. There was negative relationship between menopausal duration and BMD. Blood pressure (Systolic and diastolic) had no relationship with BMD. 80% male patient’s X-ray L-S spines finding was degenerative changes. But in female patient’s, X-ray finding nearly equally distributed in osteoporotic changes or degenerative changes or combined (Both osteoporotic + Degenerative changes) changes. BMD at the lumber spine and femoral neck level was higher for men than for women in all age groups. BMD at femoral neck level decreased for both sexes with age but reduction was lesser and later for men. BMD was higher in lumber vertebra than for femoral neck, this was because of osteophytes. Radiology was of limited value unless there was severe bone loss and compression fractures occurred. Radiology was the least sensitive method for assessing bone density.

We studied only a limited number of patient’s in an urban hospital setting lacking inadequate epidemiological date & works. So this study revealed many features which were not similar to real clinical situations in our country. On the other hand, western standard and styles are also different. On that ground, it may partially meet up the requirements to fill up the gap or better to say to add something to the bottomless ocean of knowledge.

Case No. 01

Md. Abul Kasem, 65 years, from Mohadebpur, Noagan, retired service man of bellow average body build and body weight, ex-smoker, non-diabetic, normotensive admitted on 26-02-2006 bed no P/3, RMCH, Rajshahi with low back pain and pain in the Rt. Knee. His loss of height was absent and morning stiffness for at least 1 hour was absent. He complained weight loss for 1 year. Heat intolerance was absent. His appetite was normal. Bowel habit was normal. His back pain had no radiation; duration was 21/2 months. Pain in the Right Knee joint was sudden onset and joint was swelled up and increase hotness over the joint. He was non alcoholic, His dietary habit was average. His past history was insignificant. He did not give any family history of non traumatic fracture on bones of his parent.

On examination: he was ill looking, below average body build, with anaemia, but had no jaundice, cyanosis, clubbing & oedema. His pulse rate was 76/min, rhythm was regular, character and volume was normal. His BP was 120/65 mm of Hg.

Straight leg raising (SLR) test was negative. Examination of the Rt. Knee joint revealed that temperature was increased, tenderness present, and massage test was positive. Others systemic examination was normal.

On investigation, X-ray L-S spines showed degenerative changes in the lumber spines. BMD study done by DEXA scan, showed osteoporosis in the both hips and osteopenia of the lumbar spines. This is showed in the figure A, B, C. Blood examination showed Hb%-45%, ESR-60 mm in 1st hour. Total count was normal & there was neutrophilia. C-RP was high. Serum calcium was 8.2mg /dl. RBS with CUS and serum creatinine were normal, S. uric acid was 8.5mg/dl. Features of the blood film and bone marrow can not be ruled out storage disease. No punch out lesion was seen on X-ray skull (lateral view). Urinary benze jones protein was negative.

The diagnosis was lumber spondylosis with osteoporosis of the both hips and osteopenia of the lumber spines and acute gout.

Case No: 02

Mrs. Lokjhan 70 years, housewife, from Durgapur, Rajshahi, poor socioeconomic condition, non-diabetic, normotensive, admitted in RMCH, Rajshahi, with the complaints of back pain. There was no radiation of pain, dull in nature, persistent in character, not aggravated by coughing, sneezing.    There was no history of morning stiffness for at least 1 hour. Loss of height, weight loss, and heat intolerance was absent. Appetite was normal. Alteration of bowel habit was absent. She was a non-alcoholic, non-smoker. Her dietary habit was average. She had no significant past illness. She had no family history of non-traumatic fracture of bones of her parent.

On examination, she was ill looking, below average body build with no anaemia, jaundice, cyanosis, clubbing, oedima. Her pulse rate was 70/min, rhythm was regular, character and volume was normal. Her BP was 110/65 mm of Hg.

Straight leg raising (SLR) test was negative. Examination of the other systems was also normal.

On investigation, X-ray L-S spines showed osteoporotic changes. Bone menial density (BMD) study done by DEXA scan showed osteoporosis of the both hips and lumber spines. This was shown in Fig. D, E, F. Blood Examination showed Hb%, ESR, TC, DC, normal & CPBF showed non-specific findings. Random blood sugar was normal.

The diagnosis was osteoporosis of the lumber spines and the both hips.

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