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Understanding Orthopaedics :OSTEOPOROSIS

Nilen Shah

Consultant Orthopaedic Surgeon, Bombay Hospital, Specialist in Joint Replacement and Reconstruction



The awareness of osteoporosis has grown world wide in recent years. It is being realised that osteoporosis is an extremely common condition which can cause pain and morbidity to its sufferers. Fortunately, now there are effective ways of diagnosing, quantifying the degree of severity of osteoporosis and treating it.


Osteoporosis means a condition of the bones in which there is decreased bone mass leading to an increased susceptibility of fracture. It needs to be noted that both the conditions are important viz: a decrease in bone mass and an increased susceptibility to fracture. Osteomalacia on the other hand implies that there is a defect in the bone mineralization and the bone mass even may be normal although commonly it is below normal.

Osteoporosis needs to be treated by increasing the bone mass or at least by preventing any further decrease in the bone mass so that the susceptibility to fracture is decreased. This is where the problem arises because bone mass can be accurately measured by densitometry but it is not possible to measure the susceptibility to fracture. The problems of osteoporosis are due to the actual fracture and not due to decreased bone mass or increased susceptibility to fracture. It is also further realised that the bone mass is not the only important determinant for fracture and in fact different people with the same bone mass may have different rates of fracture. This is because in osteoporosis bone may be lost from specific strategic sites which is cross-linking the bone. Due to the loss of this cross linking mechanisms of the bone, the high structural integrity of bone is lost and the bone becomes fragile. This cross linkage is lost especially with high rate of bone turnover that can be detected from bio-chemical markers.


Osteoporosis can be primary which includes senile and post-menopausal osteoporosis, the topics of discussion and secondary osteoporosis which is secondary to a specific cause such as endocrine abnormalities or steroid induced etc.

Primary osteoporosis is of two varieties

Type I or Post-menopausal : This is seen in women after the menopause and is due to the diminution of the sex hormones. There are recognised receptors on the osteoblasts which do not function optimally due to the lack of hormones. The cancellous areas of the body are predominantly affected and this classically causes Collesís fractures and compression fractures of the vertebrae.

Type II or Senile : This is seen in women as well as men commonly after 60 years of age and it is the cortical areas of bone that are predominantly affected. The osteoclasts are over-active here and the common fracture seen here is the fracture neck femur. This is the area of principal concern as it is the fracture neck femur which has the greatest degree of morbidity and mortality of geriatric fractures.


A decreased bone mass and increased fragilityof bones can be due to a low peak bone mass or increased resorption of bone or decreased formation of bone. Bone is a vital tissue and the process of resorption and formation run parallel to each other in the healthy state. However, in osteoporosis the resorption exceeds bone formation leading to a net loss of bone.

The concept of peak bone mass

The maximum bone mass in all people is obtained in the third decade and after this period bone mass is lost gradually universally. In other words, the bone mass peaks in the third decade and after this period the mass of bone gradually diminishes. It is obvious that the greater the peak bone mass achieved, the lower would be the risk of osteoporosis and its related dangers. So one effective method of treating osteoporosis is to target the people before the third decade of life and emphasise the importance of regular weight bearing exercise and diet rich in calcium and vitamin D so that maximum peak bone mass can be attained.


The diagnosis of osteoporosis can be obvious or subtle. The obvious cases are when an elderly post-menopausal lady presents with fractures of either lower end radius, vertebrae or of the femoral neck. The history is that of a relatively trivial fall. Radiographs reveal poor bone quality with reduction in the thickness of the cortices of the bone and a reduction also in the cancellous marking of the bone.

The subtle presentation may be in a middle aged man or commonly woman with various aches and pains. The site and the intensity varies. There may be such a lot of variation in the site and the intensity of the pain that one commonly thinks that there may be a functional component to the complaint. It is necessary to do blood tests and densitometry to ascertain the diagnosis in these patients.


Biochemical parameters can give an idea as to the rates of bone formation and resorption. High rate of bone turnover correlates with a low bone mass. The tests that are helpful are: CBC/ESR, s. bone chemistry i.e. s. calcium, s. phosphorus and s. alkaline phosphatase estimations. In the routine case, these are all the investigations that may be necessary. Further investigations that are relevant can be s. bone specific alkaline phosphatase, s. PTH, s. vit. D estimations and 24 hour urinary excretion of calcium and phosphorus. Interestingly, there are certain specific markers of bone resorption that are now being available namely urinary hydroxyproline and urinary pyridinolines and deoxypyridinolines. When bone is resorbed, collagen from bone is degraded into smaller units. Hydroxyproline is largely from bone but around 80 to 90% gets metabolised and the rest is excreted in urine. Unfortunately, dietary collagen and gelatin can also add to urinary hydroxyproline and therefore for proper measurements urinary sample should be obtained after at least 12 hours of fasting. Unlike hydroxyproline, urinary pyridinoline and deoxypyridinoline cross-link stabilise the collagen in extra-cellular matrix. Deoxypyridinoline cross-link is derived exclusively from skeletal tissue and is one of the most sensitive indicator of bone resorption as it does not undergo any metabolism in the body and the whole amount derived from skeletal tissue is excreted in the urine. Other assays that are being developed are tartarate resistant acid phosphatase and glycosylated hydroxylysine as immunoassays for collagen degradation.

Estimation of bone mass by bone densitometry

The modalities available are:

  1. Radiographic
  2. Single energy X-ray absorptiometry
  3. Dual energy X-ray absorptiometry (DEXA)
  4. Quantitative computerised tomogram
  5. Quantitative ultrasonography

Of all the modalities it is accepted that dual energy X-ray absorptiometry or DEXA is the most accurate and the most reproducible of the tests. However, there is poor correlation between the various skeletal sites and DEXA studies need to be done at the lumbar spine level and the hip. Quantitative USG when used for the calcaneum has the correlation of approximately 0.80 to 0.85 with DEXA. The advantage of USG is that the machine is portable and the examination can be performed relatively cheaply. However, the gold standard remains the DEXA which measures the bone mineral content (BMC) and also the bone mineral density (BMD in g/cm2)

Interpretation of BMD report

As DEXA is becoming commoner a few principles of understanding of DEXA report would be in order. The report consists of the Z score and the T score.

Z score

In this score, the patientís BMD is compared with the mean value for individuals of the same age. A low Z score indicates an aetiology other than age related bone loss and the score is expressed as standard deviation.

T score

In this score, the patients BMD is compared with the mean value for young adults of the same gender and race. Even this score is expressed as standard deviation.

The World Health Organisation has classified osteoporosis on the basis of T scores as follows:

Normal : T score is > - 1, this means that the patientís BMD is within 1 SD of the mean value for young adults of the same gender and race.
Osteopenia : T score is < - 1 but > -2.5; this means that the patientís BMD is more than 1 SD but not more than 2.5 SD below the mean for young adults.
Osteoporosis : T score is <-2.5; this means that the patientís BMD value is more than 2.5 SD below the mean or young adults.
Severeosteoporosis : T score < -2.5 and with at least one fragility fracture.

By this definition, 70% of women over the age of 80 years who are untreated have osteoporosis.

Bone biopsy

When diagnosis remains in doubt a transiliac bone biopsy will be useful but care needs to be taken to ensure that the bone is not crushed by the biopsy procedure.


The treatment of osteoporosis can be pharmacological and non-pharmacological.

Non-pharmacological treatment of osteoporosisExercise and life style

It is well recognised that regular weight bearing exercise helps not only in prevention of osteoporosis but also in its treatment. Regular walks and gentle exercises of the whole body are extremely important for osteoporosis.

Life style changes in the form of avoidance of smoking and in our country especially stopping pan parag or other guthakas are important for treatment of osteoporosis. Alcohol intake also need to be curtailed.

Modification of external environment

The problems of osteoporosis arise not due to osteoporosis per se but due to its complication viz; fracture. It is sensible to prevent fractures by providing a safer environment. This can take the shape of hip protectors (Devices that are worn on the hip region to decrease the impact of the fall) or providing surfaces that absorb shocks and region to decrease the impact of the fall) or providing surfaces that absorb shocks and decrease theamount of force that is transmitted to the hip. Obviously these sort of modifications are possible only in homes for the elderly and in institutions. There is evidence that when these changes have been made the rates of fractures have decreased. Due to the availability problems, at present these options are not fully utilised in India.

Pharmacological treatment

Calcium and vitamin D supplementation

It has been shown by various studies that supplementation with calcium and vit. D can retard, stop or even reverse bone mass on serial bone densitometry studies. However, although there is evidence that by supplementation of these nutrients even the fracture rate is reduced the evidence is not absolutely convincing. In a large prospective study involving 3300 patients, randomised to receive either a placebo or 800 IU of vit. D and 1.2 g of calcium/day, for three years; it was found that 20 of the treatment group had fractures compared to 37 of the placebo group. It should be noted that fractures can not be prevented altogether, although the rates can be reduced by providing life long supplementation with calcium and vit. D. One other point that is worth noting in clinical practice is that there is no real advantage in providing active form of vit. D with its increased costs unless there is evidence that there is a renal problem with a hydroxylation defect resulting in failure of conversion of inactive to active form of vit. D.

Oestrogen therapy

It has been shown in over more than 20 studies that oestrogens will prevent post menopausal bone loss which on an average may be between 1% (slow losers) to 3 to 5% (rapid losers) per year. The oestrogens may be supplied in the form of conjugated oestrogens 0.625 mg/day or oestradiol 2 mg/day or an oestrogen patch providing 50 microg/day. In all nonhysterectomised women, progestagen must be added together with oestrogen therapy.

Most of the studies have been done on recent postmenopausal women and there is scanty evidence that the protective effect of oestrogen will also be present if they are started some years after menopause. Moreover, the effect of oestrogen lasts for current users only and rapidly declines to control levels after stopping oestrogens. Oestrogens can safely be used for 10 years although gynaecologic consultations and mammography will become necessary.


These are chemical agents that can inhibit osteoclasts without having any inhibitory effect on the osteoblasts thereby producing net bone gain. They have a definite role in which there is osteoclast mediated increased bone resorption such as in hyperparathyroidism, Pagetís disease or malignant hypercalcaemia. Etidronate and Alendronate are the two agents that have been used for osteoporosis.

Etidronate in randomised studies has failed to show a significant difference between placebo and treated groups in fracture rates. However, alendronate in similar prospective randomised double-blind trials has shown a decrease in the frequency of vertebral and Collesís fractures in the treated groups. The reduction in the frequency of hip fractures has not been that spectacular. However, alendronate has been available in the market and in clinical use only for the last few years and data regarding its long-term safety is lacking. The recommendation is to use it for 3 years whereby the bone mineral density would increase by around 10% and then not use it for 1 year and then re-use it for another 3 years. It should also be noted that the benefits of alendronate will only be seen if it is continued at least for a period of 2 years. Alendronate should be taken on an empty stomach with water and nothing should be ingested for at least half an hour to allow its absorption.

Other pharmaceutical measures

Fluoride and calcitonin have also been used.
Fluoride increases bone mass but the bone formed is abnormal and is more prone to fractures. Calcitonin can increase the bone mass but its relationship with fracture reduction is not ascertained.

Anabolic steroids have also been used but their effect on increasing the bone mass is not definite although they do increase muscle mass.

Drugs still under evaluation

PTH in low doses intermittently can increase cancellous bone mass but causes a decrease in cortical bone. Hence, PTH in such doses combined with antiresorptive agents, is being evaluated.

Thiazide diuretics decrease the urinary excretion of calcium and can increase the bone formation.

Oestrogen analogues such as raloxifene and droloxifene which act as agonists for bone but antagonists for breast are thought to hold promise for the future.

Treatment recommendations

Post menopausal women till around 10 years post menopause should be offered hormone replacement therapy. Gynaecologic consultation and mammography should be performed once a year. This can be given for 10 years and there is evidence that there is no increased risk of breast cancer for the doses recommended and if used only for 10 years.

In women who do not tolerate HRT and in men with osteoporosis alendronate is the drug of choice and it should be used at least for 2 years and then not used for 1 year and used again for 2 years. Calcium and vitamin D supplementation should be given to all. The newer active forms of vitamin D are necessary only if there is a renal defect and inability of the body to convert inactive to active forms.


A lot of progress has been made in understanding of osteoporosis and rapid strides are being made in its treatment. There is evidence that bone can be made stronger by treatment for osteoporosis, so that there is a decreased susceptibility to fracture. However, this susceptibility as yet can not be totally reduced as there are multiple factors as to why a bone fractures. Treatment for osteoporosis will only be effective if it is informed and the patients realise its role and limitations.

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