Osteoporosis often whispers before it breaks — a gentle check today can prevent a life-changing fracture tomorrow.

How common is osteoporosis and fractures in India?

• Around 60 million Indians are estimated to have osteoporosis; the majority are women. The peak occurs earlier than in many Western countries.
• Hip fractures: community and hospital studies estimate the annual hip-fracture incidence in people aged >50 years in India at roughly 120–130 per 100,000 (crude; higher in women). Projections suggest a large and rising burden as the population ages.
• Vertebral (spine) fractures: population studies (for example the Delhi Vertebral Osteoporosis Study) report vertebral fracture prevalence ~18% in people >50 years — vertebral fractures are common and often silent.

Who is at risk?

• Older age (especially >65) and postmenopausal women.
• Low body weight, small frame.
• Family history of hip fracture.
• Previous fragility fracture (fall from standing height).
• Long-term use of glucocorticoids, some anti-seizure medicines, aromatase inhibitors (used for treating breast cancer).
• Smoking, excess alcohol, poor mobility or frequent falls.
• Low calcium/vitamin D intake, poor sunlight exposure, and low protein intake.
• Secondary causes: rheumatoid arthritis, hyperparathyroidism, chronic kidney disease, thyroid disease.

What are the risk factors?

• Non-modifiable: age, sex (female), prior fracture, family history of hip fracture.
• Modifiable: smoking, alcohol, low physical activity, low calcium intake, vitamin D deficiency, frequent falls, polypharmacy (sedatives).
• Secondary causes (screen for): prolonged steroids, hypogonadism, hyperparathyroidism, thyroid disease, growth hormone deficiency, chronic liver/renal disease.

How do doctors make the diagnosis? — A simple pathway

1. Clinical assessment: age, prior fractures, medicines (e.g., steroids), family history, falls, lifestyle.
2. Secondary workup if needed: basic blood tests (calcium, vitamin D, TSH, creatinine), review of medicines and/or further endocrine tests.
3. FRAX risk assessment: an easy online calculator that estimates a person’s 10-year fracture risk (major osteoporotic fracture and hip fracture) using clinical risk factors — can be used with or without a DEXA result. FRAX has India-specific considerations and thresholds.
4. Bone mineral density (BMD) by DEXA (DXA): measures areal BMD at the hip and spine and gives a T-score. Osteoporosis is conventionally diagnosed when T-score ≤ −2.5 (postmenopausal women / men >50) — but remember: treatment decisions use both BMD and clinical risk.
5. Bone markers: e.g. bone formation markers (e.g. PINP) and bone resorption markers (beta cross laps CTX telopeptides).

Role of DEXA — why it matters (and its limits)

• Why DEXA helps: hip and spine BMD are the best single standard test to quantify bone mass, monitor response to treatment, and refine FRAX risk when combined with clinical factors.
• Pitfalls and limitations: Degenerative spine disease, vertebral osteophytes, aortic calcification or prior spinal surgery can falsely increase spine BMD and hide true fracture risk. Always inspect images and, if needed, use hip BMD or alternative sites.
• Machine and site variability: different DXA machines and centres may give slightly different values — use the same centre for follow-up when possible and follow recommended least-significant-change thresholds.
• Areal BMD ≠ bone quality: DEXA measures density, not microarchitecture. Tools like Trabecular Bone Score (TBS) or advanced imaging (QCT) can add information in selected patients.

FRAX — the risk calculator (how to use it simply)

• FRAX calculates the 10-year probability of a major osteoporotic fracture and hip fracture using age, sex, weight/height, prior fracture, parental hip fracture, smoking, glucocorticoids, RA, secondary osteoporosis, alcohol, and optionally femoral neck BMD.
• In India FRAX inputs and treatment thresholds should be interpreted with clinical judgement; FRAX is a decision-aid not a rule. Use FRAX especially when DEXA is unavailable or to combine DEXA + risk factors.

Treatment options: Antiresorptives (slow bone loss) — first line for many

• Bisphosphonates (oral alendronate, risedronate; IV zoledronate): reduce hip/vertebral fractures, often first-line for many patients. Good for long-term fracture prevention.
• Denosumab (monoclonal antibody to RANKL): powerful antiresorptive given by 6-monthly injection — increases BMD and lowers fractures. Important: stopping denosumab can cause rapid loss of gains and rebound vertebral fractures unless patients are transitioned to another antiresorptive (usually a bisphosphonate). Discuss long-term plan before starting.

Treatment options: Osteo-anabolics (build new bone) — for high-risk or severe cases

• Teriparatide (PTH analogue) — daily injections for up to 2 years — stimulates bone formation, reduces vertebral fractures.
• Romosozumab (sclerostin inhibitor; anabolic then antiresorptive effect) — given monthly for 12 months; shows rapid BMD gains and fracture reduction (pivotal FRAME and ARCH trials). After romosozumab, follow quickly with an antiresorptive to maintain gains. There are cardiovascular considerations in some patients — treatment decisions must be individualized.

Practical sequencing point: For very high fracture risk (multiple prior fractures, very low BMD), start with an anabolic (romosozumab or teriparatide) then switch to an antiresorptive to consolidate gains. For many patients, long-term antiresorptive therapy is then continued.

Safety points & monitoring

• Atypical femoral fracture (AFF) — rare; risk increases with long-term bisphosphonate use; periodic reassessment and drug holidays may be appropriate for select patients.
• Osteonecrosis of the jaw (ONJ) — rare, more common with invasive dental procedures while on high-potency antiresorptives; dental review before starting certain therapies is prudent.
• Rebound fractures after stopping denosumab — plan transition therapy (usually a bisphosphonate) to prevent rapid bone loss.
• Caution in patients with poor kidney function and/or history of abnormal heart rhythms.
• Romosozumab: evaluate cardiovascular history; discuss risks and benefits if atherosclerotic cardiovascular disease is present.

Follow-up & monitoring should be undertaken no later than 3 months.

Lifestyle — what really helps

• Protein: older adults should aim for ~1.0–1.2 g/kg/day of good quality protein to help maintain muscle and bone (higher if illness; but adjust if advanced kidney disease). Spread protein through the day.
• Calcium and vitamin D: aim for ~1000–1200 mg calcium/day (food + supplements if needed) and vitamin D supplementation (many older adults benefit from 800–1000 IU/day; test and correct deficiency). Discuss with your doctor before starting supplements.
• Exercise: weight-bearing and resistance training (walking, stair climbing, resistance bands/weights) 3–5 times weekly + balance training to reduce falls.
• Fall prevention: home safety (remove rugs, improve lighting), vision and hearing checks, treat dizziness/orthostatic symptoms.
• Avoid smoking and limit alcohol. Both increase fracture risk.

Our research in this area

Peer-reviewed publications and conference presentations by Dr. Vishal Gupta and colleagues.

1. Gupta V. Normocalcemic primary hyperparathyroidism in a patient with severe osteoporosis receiving teriparatide. Indian J Endocrinol Metab 2013;17(2):336–338. PMID:23776916. PMCID:PMC3683218. doi:10.4103/2230-8210.109664
2. Cheng ML, Gupta V. Premenopausal osteoporosis. Indian J Endocrinol Metab 2013;17(2):240–244. PMID:23776895. PMCID:PMC3683197. doi:10.4103/2230-8210.109681
3. Gupta V, Shah MA, Shah SK, Shah JM. Osteoanabolics. Indian J Endocrinol Metab 2012;16(3):349–357. PMID:22629498. PMCID:PMC3354839. doi:10.4103/2230-8210.95662
4. Cheng ML, Gupta V. Teriparatide — indications beyond osteoporosis. Indian J Endocrinol Metab 2012;16(3):343–348. PMID:22629497. PMCID:PMC3354838. doi:10.4103/2230-8210.95661
5. Gupta V, Patil S, Shah D. Primary hyperparathyroidism associated with vitamin D toxicity in a patient with severe osteoporosis receiving teriparatide. Indian J Endocrinol Metab 2012;16(5):863–864. PMID:23087890. PMCID:PMC3475930. doi:10.4103/2230-8210.100697
6. Gupta V. Vitamin D: extra-skeletal effects. J Med Nutr Nutraceuticals 2012;1(1):17. doi:10.4103/2278-019X.94632
7. Gupta V. Simultaneous presentation of giant pheochromocytoma, primary hyperparathyroidism, and mixed-medullary-papillary thyroid cancer in MEN 2A. Indian J Endocrinol Metab 2013;17(4):751–755. PMID:23961501. PMCID:PMC3743385. doi:10.4103/2230-8210.113776
8. Gupta V, Sunavala AJ, Bhansali S, Kakkar R. Parathyroid storm secondary to parathyroid adenoma presenting as acute necrotizing pancreatitis. The Endocrinologist 2009;19(1):6–8. doi:10.1097/TEN.0b013e3181939504