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Osteoporosis: Current Concepts

Pankaj Kumar*

*Assistant Professor, Department of Orthopaedics, B.P.Koirala Institute of Health Sciences, Dharan, Nepal

Address for Correspondence:

Pankaj Kumar
Assistant Professor, Department of Orthopaedics
B.P.Koirala Institute of Health Sciences, Dharan , Nepal
Ph No:  00977-25-525555-3260,2016
Fax No: 00977-25-520251

J.Orthopaedics 2007;4(3)e3


Osteoporosis is characterized by decreased bone mass and increased susceptibility to fracture. The World Health Organization defined Osteoporosis in 1994 as a condition in which the bone mineral density (BMD) is 2.5 SD or more below the mass for young healthy adults of the same race and gender - also referred to as a T- score of – 2.5.  Those who fall at the lower end of the normal range (a negative  T –score of > 1 SD)  are defined as having low bone density and are considered to be at increased risk of osteoporosis.


By this definition a quarter of all post- menopausal American Caucasians, in total 26 million white American women are regarded as having osteoporosis. Osteoporosis occurs more frequently with increasing age, as bone tissue is progressively lost. In women, the loss of ovarian function at menopause (typically about age 50) precipitate rapid bone loss such that most women meet the diagnosis criteria for osteoporosis by age 70 to 80. Fractures of distal radius increases in frequency before age 50 and plateau by age 60, with only a modest age–related increase thereafter. In contrast, incidence rate for hip fracture double every 5 years after 70. The rising burden of those fractures imposes an enormous cost on society and increases morbidity and mortality. A fracture of the hip is associated with a reduction of 20% in expected survival. Many patients become permanently disabled with the proportion who cannot walk rising from 20% before to 50% after fracture. One third totally, necessitating institutionalization.  

                       It is therefore, imperative to implementation strategies for preventing such fractures in the community. The purpose of the present lecture is to review the pertinent information regarding the biological characteristics, physiological evaluation, treatment and prevention of osteoporosis.


Osteoporosis results from bone loss due to normal age related changes in bone remodeling as well as extrinsic and intrinsic factors that exaggerated this process. These changes may be superimposed a low peak bone mass. Consequently understanding the bone remodeling process is fundamental to understanding the Pathophysiology of osteoporosis. The skeleton increases in size by linear growth and by apposition of new bone tissue on the outer surface of the cortex. This latter process is called “ modeling “. A process that allows the long bones to adapt in shape to the stress placed upon them. Bone remodeling has two primary functions: - A) to repair micro damage within the skeleton to maintain skeletal strength and B) To supply calcium from the skeleton to maintain serum calcium.  

Remodeling may be activated by micro damage to bone as a result of excessive or accumulated stress. Acute demands for calcium involve osteoclast- mediated resorption as well as calcium transport by osteocytes. Bone remodeling is also regulated by several circulating hormones, including estrogen, androgens, vit-D and PTH, as well as locally produced growth factors such as IGF-I and IGF-II transforming growth factor (TGF) ß parathyroid hormone related peptide (PTHr P) ILs, prostaglandin and tumor necrosis factor (TNF). The cytokine responsible for communication between the osteoblast and osteoclast has been identified as RANK or osteoprotegerin ligand. The osteoclast receptor for this protein is referred as RANK. Additional influences include nutrition (particularly calcium intake) and physical activity level. The end result of this remodeling process is that the resorbed bone is replaced by an equal amount of new bone tissue. Bone remodeling proceeds throughout life and an imbalance in this process that either enhances resorption or impairs formation ultimately leads to a net loss of bone mass.

Calcium Nutrition: - Calcium is an essential mineral that participates in many important physiological functions. Calcium requirements change throughout life depending on the activity and functions of the body as well as on the efficiency of intestinal absorption. 1,2,3,4 During the adult phase of life, insufficient calcium intake induces secondary hyperparathyroidism and an increase in the rate of remodeling to maintain normal serum calcium levels. PTH stimulates the hydroxylation of vit-D in the kidney, leading to increased level of 1, 25-dihydroxy vit- D 1,25(OH) 2 D and inhanced gastrointestinal calcium absorption.

The greater the peak bone mass achieved, the better the chance of avoiding osteoporosis later in life. After peak bone mass reached, bone loss normally occurs at the rate of 0.3% per year in man and 0.5% per year in women. A rate of bone loss of 2 to 3% per year (an 8% decrease in trabecular bone and a 0.5% decrease in cortical bone) begins at the onset of menopause. This rate continues for a period of 6 to 10 year and then declines to the rate of 0.5% per year. While all adults lose bone with age, osteoporosis develops in only 20 to 30% of women and 10 to 20% of men who are more than sixty-five year old.5, 6

Vit-D: Vit D plays major role in calcium metabolism.7 Vit-D is formed from 7- dihydrocholecalciferol in the skin under the direct stimulation of UV light. The vit-D precursor is converted to 25 hydroxy vitamin D in the lever before being activated by further hydroxylation to 1, 25 dihydroxyvitamin-D in the kidneys in response to parathyroid hormone. 1, 25- dihydroxyvitamin-D increase absorption of calcium across the gut by maturing the villus lining cells of the intestine and stimulating them to produce calcium-binding protein. Active vit-D augments parathyroid recruitment of osteoclast for bone resorption by acting as a maturation hormone for the macrophage stem cells.

Parathyroid hormone:  The second prominent hormone in the bone metabolism is parathyroid hormone. Parathyroid hormone responds to low ionic calcium levels by stimulating the retention of calcium and excretion of phosphate by the kidney.

Calcitonin: Calcitonin is a calcitropic peptide produced in the Para follicular cells of the thyroid gland. Calcitonin responds to elevated serum ionic calcium levels by decreasing the number and activity of osteoclast.8 Calcitonin also functions as a neuropeptide and has analgesic effect. Pharmacological activity primarily decreases bone resorption.

Estrogen: Young woman who has episodes of amenorrhea or oligomenorrhea before peak bone mass is attained lose 2% of bone mass per year, instead of gaining 2 to 4% per year as they would normally. This loss is estrogen dependent and the bone mass that is lost is not regained once normal menstrual cycles are resumed.9, 10

Glucocorticoids: Exogenous administered corticosteroid impair the function and shorten the life span of osteoblast and contribute to decreased bone formation. Coticosteroids increase the excretion of calcium in urine and block the resorption of calcium in gut. That induces hyperparathyroids. The result is a form of osteoporosis.11

Thyroid Hormone:  Thyroid hormone increases bone remodeling with osteoclast activity predominating inducing a net loss of bone.12

Approach to the pateint :

The evaluation of a patient in whom osteoporosis is suspected should include a through medical history and physical examination should be performed to identify risk factors for osteoporosis.

Risk for osteoporosis: If the patient has a facture that was not due to noticeable trauma the clinician first must rule out the presence of a benign, metastatic or primary malignant bone tumor. Once a tumor has been excluded, the major causes of such a fracture include bone-marrow abnormalities, endocrinopathies, osteomalasia and osteoporosis. The clinician should seek to identify include early natural or operatatively induced menopause, prolonged period of amenorrhea, poor nutrition, a history of limited exercise, genetic factors and a history of alcohol intake or smoking.  

Laboratory Studies:  Laboratory studies are used to exclude other disease that can cause osteopenia and to determine the type of osteoporosis. 

Imaging studies and the measurement of bone mineral density

Measurement of bone mineral density can be used to access the risk of a fracture with high degree of specificity. There is a 1.5 to 3-fold increase in the fracture rate for each standard deviation of decrease in bone mineral density.13

            Radiograph of the spine demonstrate osteopenia (a radiographic term for an apparent decrease in bone mass density) only when 30% of the bone mass has been lost. The preferential loss of horizontal trabeculae in vertebral body gives the remaining vertebral trabecular a hypertrophic appearance.

                      Single –beam densitometry can be used to measure bone mass at the distal third of the forearm.14 The finding at that location may not correspond with the changes in the spine or the hip.

CT scanning can be used to exmine a window within the vertebral body as well as to measure the trabecular bone mass therin.Among radiograph methods,it is most sensitive to changes in bone mass; however it is less precise, is more costly and results in a higher exposure to radiation than dual-energy absorptiometry.15

DEXA (  Dual energy x-ray absorptiometry) has a high rate of precision and subjects the patients to an extremy low dose of radiation.It currently the most frequently used method of evaluating bone density in clinical practice.

Bone Biopsy: Tetracycline labeling of the skeleton allows determination of the rate of remodeling as well as evaluation for other metabolic bone diseases. The current use of BMD test, in combination with hormonal evaluation and biochemical markers of bone remodeling, has largely replaced bone biopsy.


Non-pharmacological prevention of osteoporosis:

Nutrition: The role of calcium in attaining an adequate peak bone mass and reducing age-related bone loss has been thoroughly investigated. In spite of all published data there is no universal agreement as to the required daily intake of calcium. In 1994 a consensus conference recommended a daily intake of 1200 to 1500 per day, 1000 mg. for adults up to 65 year and 1500 mg. for post-menopausal woman.16 Absorption of calcium is dependent on the level of vit-D.

Physical Activity: The frequency of falls is the most potent risk for fractures. A recent prospective RCTs have shown that exercise can reduce the risk of falling in elderly.17, 18

Bone responds to exercise less in adulthood than during growth. In the adult and after the menopause, physical activity should be regarded as bone-preserving rather than bone building. Several studies and RCTs have shown that exercise increases the BMD by few percentage points at best.19, 20

Hip protectors:  Energy absorption in the soft tissue around the hip has been shown to protect against fractures of the hip. Partly explaining why the overweight has fewer such injuries.21  

Pharmological prevention of osteoporotic fractures:

Calcium and vit-D- Calcium supplement, generally in a dose of 500 mg to 1000 mg. daily is known to slow the rate of loss of BMD in elderly patients with a low calcium intake.22, 23 Calcium in conjunction with vit-D has been shown to reduce the incidence of hip fracture in elderly dwellers in nursing home.

An RCT carried out in France included women living in care homes who were treated daily for three years with 1200mg of calcium and 800 IU of vit-D. They had a reduction in fractures of the hip of 29% and fewer non-vertebral fracture 24% compared with placebo group.24, 25

One recent meta-analysis included showed that vit-D did not reduce the risk of fractures, but in combination of calcium, the risk was reduced by 26% in elderly patients living in care home.26

Hormone replacement therapy:

Several small RCTs have supported the view that estrogen increases the BMD over a period of one to three years by a few percentage points and reduced the risk of fracture in the spine by about 50%. 27

One meta-analysis: showed that reduction of 33% in vertebral fracture by HRT.

However HRT has many serious adverse effects, including vaginal bleeding, breast tenderness, deep vein thrombosis and pulmonary embolism, stroke, heart disease and gall bladder disease and increased risk of breast endometrial and ovarian cancer after long-term use. 28 On this basis estrogen is not recommended currently as the primary prevention of osteoporosis in most countries.

Selective estrogen receptor modulator (SERM)

A selective receptor modulator (SERM) such as raloxifene is an antagonist of estrogen in the breast and the endometrium but an agonist in bone and lipid metabolism. Raloxifene also lowers the frequency of breast cancer by 70% 29 but increase the incidence of venous thrombosis and pulmonary embolism at a similar rate as HRT.30

As new SERMs are under development in phase III trails their numbers will probably expend in the future.  

Bisphonates: A recent meta- analysis with use of Etidronate showed that reduction of vertebral fractures by 40%. Whereas no effect on other fractures.31

Alendranate is another bisphonate in which RCTs have shown a reduction in hip Fractures by 51% and vertebral fracture 47% as compared with placebo treatment. The dose was 5 mg daily for 2 years followed by 10 mg daily in third years.32

A recent metaanalysis showed that daily use of 10 mg of alendronate, which reduce the vertebral fracture by 48% and non- vertebral fractures by 49%. 33 Metaanalysis with Reserdronate showed that reduces the vertebral fractures by 36% and non –vertebral fractures by 27%. 34

Calcitonin: A recent metaanalysis evaluating calcitonin showed reduces the incidence of vertebral fractures by 54%. 35 The daily 200 IU of intranasal salmon calcitonin/day reduce the risk of vertebral fractures by 31% but no effect on peripheral fractures.36

Parathyroid Hormone:Intermittent injection of PTH in individuals with osteoporosis stimulates the formation of bones, increases the BMD and reduces the risk of fractures.37

Strontium- A recent RCTs suggested that 2 mg of strontium /day over 3 years reduces the risk of sustaing a new vertebral fractures by 49% during the first year and by 41% during the entire period.38

Other Drugs- Fluoride is incorporated into the hydroxyapetite crystal of bone. It stimulates recruitment and activity of osteoblast increases the BMD in spine and to a less extent in the hip.39 Alphacalcidol and calcitrol are vit-D analogues, which have been shown to increase the BMD.40 Menatetrenone, a vit-K2 compound, has been shown to omprove theBMD.41

The Role of Orthopaedic Surgeon

Orthopaedics surgeon sees many patients with osteoporosis. It is silent disease without any preceding symptoms until the first fractures occur. Evaluation of patients must therefore include a history of risk factors and BMD scan. It is the responsibility of the Orthopaedics surgeon to arrange for patients to be properly adviced and investigated for osteoporosis.  

Synopsis of Major Recommendations To The Physician

* Counsel all women on the risk of osteoporosis and related fractures.

* Advise all patients to consume adequate amounts of calcium (at least 1200 mg   /day, including supplements if necessary) and vit-D (400 to 800 IU /day for individuals at risk of deficiency)

* Recommended regular weight – bearing and muscles –strengthening exercise to reduce the risk of falls and fractures.

* Advice patients to avoid tobacco smoking and excessive alcohol intake.

* Recommend BMD testing to all women aged 65 and older.

* Recommended BMD testing to postmenopausal women who have suffered a fragility fracture to conform the diagnosis and determine disease severity.

* Initiate therapy to reduce fracture risk in postmenopausal women with BMD T- scores by central dual X-ray absorptiometry (DXA) below –2 in the absence of risk factors and in women with T- scores below –1.5 if one or more risk factors is present.

* Consider postmenopausal women with vertebral or hip fractures candidates for osteoporosis treatment.

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Please cite as :Pankaj Kumar : Osteoporosis: Current Concept

J.Orthopaedics 2007;4(3)e3





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