Osteoporosis: Symptoms, Diagnosis, Treatment and Prevention

Rheumatology ·

Osteoporosis: Symptoms, Diagnosis, Treatment and Prevention

Osteoporosis is called a "silent epidemic" — and the name fits precisely. Bone deteriorates for years without a single symptom, and the first signal is a fracture: from a minor knock, an awkward twist, or even a forceful cough. One in three women over 50 and one in five men of the same age will sustain an osteoporotic fracture in their remaining lifetime. The good news: the disease can be detected long before that moment — and its progression significantly slowed.

What Is Osteoporosis and How Does It Develop

Bone is living tissue in a constant state of renewal. Specialised osteoclast cells break down old bone while osteoblasts build new tissue. Normally these processes are balanced and bone maintains its strength. Peak bone mass is reached around age 25–30 — this is a kind of "bone capital" for the rest of life. After age 30–35 the balance gradually shifts: breakdown begins to outpace formation and bone density slowly declines.

Osteoporosis is the point at which bone loss has progressed far enough that bone becomes brittle and fractures under loads that healthy bone would withstand with ease. Bone microarchitecture is disrupted: trabecular struts thin and perforate, and the bone begins to resemble moth-eaten sponge.

Two main types are recognised:

  • Primary osteoporosis — postmenopausal (type I, in women in the early years after menopause when oestrogen falls) and senile (type II, in men and women over 70)
  • Secondary osteoporosis — a consequence of another disease (e.g. rheumatoid arthritis) or drug treatment: glucocorticoids, antiepileptics, aluminium-containing antacids

Symptoms of Osteoporosis: Why the Disease Is Missed for Years

Osteoporosis itself does not hurt. This is precisely what makes it so dangerous — while bone density falls, the person feels entirely well. Early indirect signs worth noting:

  • Loss of height — losing more than 2–3 cm compared to young adult height suggests vertebral compression fractures, which often occur silently
  • Chronic back pain — especially in the thoracic and lumbar spine; may be the result of "quiet" vertebral fractures
  • Posture changes — progressive thoracic kyphosis ("dowager's hump"): vertebrae gradually deform wedge-shaped under body weight
  • Fractures from minimal trauma — wrist from a fall from standing height, hip during walking, ribs from a hug

Hip fracture is the most severe complication. In elderly patients it is associated with high mortality in the first year: up to 30% of patients die from complications (thromboembolism, pneumonia, heart failure) — not from the fracture itself, but from the prolonged immobilisation that follows.

Low Bone Density Causes and Risk Factors

Bone loss is a universal ageing process, but the rate and severity are shaped by a combination of factors.

Risk factor Mechanism
Female sex and menopause Oestrogen brakes osteoclast activity; its fall at menopause accelerates resorption 3–5 fold
Age over 65 Reduced cutaneous vitamin D synthesis, impaired calcium absorption, sarcopaenia
Family history Genetics determines up to 60–80% of peak bone mass
Low oestradiol / testosterone Sex hormones protect bone in both sexes
Low body weight (BMI < 18.5) Less mechanical load on bone; less adipose tissue for oestrogen synthesis
Smoking Accelerates oestrogen breakdown, impairs bone blood supply
Alcohol (> 2 units/day) Direct toxicity to osteoblasts; impairs calcium absorption
Glucocorticoids (prednisolone > 3 months) Suppress osteoblasts and intestinal calcium absorption
Sedentary lifestyle Bone strengthens under mechanical load — without it, it atrophies
Calcium and vitamin D deficiency Impaired mineralisation of newly formed bone

Diagnosing Osteoporosis: Densitometry and Blood Tests

Densitometry (DXA — dual-energy X-ray absorptiometry) is the diagnostic gold standard. It measures bone mineral density (BMD) at the lumbar vertebrae and femoral neck. The result is expressed as a T-score — the deviation from peak bone mass in young adults:

T-score Interpretation
Above −1.0 Normal
−1.0 to −2.5 Osteopaenia (reduced density preceding osteoporosis)
−2.5 and below Osteoporosis
−2.5 and below + prior fracture Severe osteoporosis

Densitometry is recommended for all women over 65, men over 70, and younger individuals with risk factors (menopause before 45, glucocorticoid use, prior fragility fracture).

Blood tests are needed to exclude secondary osteoporosis and assess calcium-phosphate metabolism before starting treatment:

  • Calcium — total and ionised. Usually normal in primary osteoporosis; marked elevation points to hyperparathyroidism.
  • Vitamin D (25-OH) — essential. Vitamin D deficiency is one of the most frequent correctable risk factors; at levels below 30 nmol/L, bone mineralisation is impaired.
  • Parathyroid hormone (PTH) — elevated in secondary hyperparathyroidism (response to calcium/vitamin D deficiency) and in primary hyperparathyroidism as an independent cause.
  • Phosphorus — reduced in osteomalacia and several forms of secondary osteoporosis.
  • Oestradiol in women / testosterone in men — when hormonal deficiency is suspected as the cause of bone loss.
  • Bone turnover markers — osteocalcin (formation) and β-CrossLaps/CTX (resorption) — used to monitor treatment response.

Treating Osteoporosis: Medications and Lifestyle Measures

Treatment is started at T-score −2.5 or below, and also in osteopaenia when the 10-year fracture risk calculated by the FRAX tool is high.

Baseline therapy — nothing else works effectively without it:

  • Calcium 1000–1200 mg/day as elemental calcium — from food and supplements as needed
  • Vitamin D3 800–2000 IU/day (dose guided by 25-OH vitamin D blood level)

Antiresorptive therapy — slows bone breakdown:

  • Bisphosphonates (alendronate, zoledronate, ibandronate) — first line; reduce vertebral fracture risk by 40–70%, hip fracture by 40–50%
  • Denosumab — monoclonal antibody blocking RANKL, the key activator of osteoclasts; used when bisphosphonates are not tolerated or in renal insufficiency
  • Hormone replacement therapy (HRT) — in women in early postmenopause; effective bone protection, prescribed with careful consideration of cardiovascular and oncological risks

Anabolic therapy — stimulates new bone formation; reserved for severe osteoporosis:

  • Teriparatide (PTH fragment) — the only agent that genuinely builds new bone
  • Romosozumab — blocks sclerostin, simultaneously stimulating formation and inhibiting resorption

Note: bisphosphonates are taken in courses with "drug holidays" — after 3–5 years of treatment a break is taken under densitometry monitoring. Do not stop or switch therapy independently.

Osteoporosis Prevention: Diet and Lifestyle

No medication works effectively against a background of calcium and vitamin D deficiency — this is the foundation without which treatment cannot reach its target.

Calcium from food — the preferred source:

Food Calcium per 100 g
Hard cheese 700–1200 mg
Milk, kefir, yoghurt 110–120 mg
Canned sardines (with bones) 380 mg
Tofu (calcium-set) 350 mg
White cabbage 48 mg
Broccoli 47 mg

Daily calcium requirement: 1000 mg for adults 18–50, 1200 mg for women over 50 and men over 70.

Exercise — one of the most underestimated treatment tools. Weight-bearing and resistance training stimulate osteoblasts through mechanical stress. Effective activities: walking, running, dancing, strength training, yoga, tai chi. The last two are particularly valuable for fall prevention: they improve balance and coordination.

Swimming and cycling, despite their cardiovascular benefits, create minimal mechanical load on bone.

Fall prevention — a separate strategy, especially in older adults: removing thresholds and slippery surfaces at home, good lighting, vision correction, discontinuing sedating medications where possible.

When to See a Doctor Urgently

Osteoporosis is not an emergency condition, but several situations call for prompt medical attention:

  • Acute back pain after minimal or no trauma — possible vertebral compression fracture; X-ray or MRI of the spine needed
  • A fall with pain in the hip, groin or thigh — suspected hip fracture; immediate hospitalisation required
  • Newly discovered T-score of −2.5 or below — planned but prompt assessment by a rheumatologist or endocrinologist to initiate therapy
  • Height loss of 4 cm or more — indication for spinal X-ray even in the absence of pain

Early diagnosis changes outcomes radically. Starting treatment at osteopaenia can prevent the first fracture entirely. Starting after — can prevent the next one. In either case, starting now is the right call.

This article is for informational purposes only. Diagnosis and choice of therapy are the responsibility of a rheumatologist or endocrinologist.

Frequently Asked Questions

A DXA bone scan cannot be fully replaced — it is the only tool that precisely measures bone mineral density. However, blood tests complement the picture: levels of calcium, vitamin D and parathyroid hormone can reveal disturbances in calcium-phosphate metabolism that accelerate bone loss. For an initial estimate of 10-year fracture risk, the online FRAX calculator can be used — it factors in age, sex, weight, smoking, steroid use and family history.

For bone health, 25-OH vitamin D should be at least 50 nmol/L (20 ng/mL). The optimal range is 75–125 nmol/L. Below 30 nmol/L, intestinal calcium absorption is impaired and secondary hyperparathyroidism is stimulated — which directly accelerates bone loss. Details on reference ranges and interpretation in the vitamin D article.

Complete restoration of lost bone mass is not possible. However, modern therapy can halt further loss and significantly reduce fracture risk. Anabolic agents such as teriparatide can genuinely build new bone — some patients see T-score improvements of 0.5–1.0 within a year of treatment. The key goal is to prevent the first major fracture, since it sets off a chain of complications.

Osteopaenia is a T-score between −1.0 and −2.5 — reduced bone density that precedes osteoporosis. The condition itself does not cause fragility fractures, but it is a warning: without lifestyle correction and in the presence of risk factors, it progresses to osteoporosis. Drug treatment is not always indicated — the doctor assesses the overall 10-year fracture risk using the FRAX scale.

After menopause, oestrogen levels fall sharply. Oestrogen normally suppresses osteoclast activity — the cells that break down bone. Without its protection, bone resorption accelerates 3–5 fold, and a woman can lose 20–30% of bone mass in the first 5–7 years after her last period. In men, testosterone partially converts to oestrogen, so bone loss is slower and occurs later.

Alcohol in large amounts is directly toxic to osteoblasts and impairs calcium absorption. Smoking accelerates oestrogen metabolism and reduces bone blood supply. Excess dietary sodium increases urinary calcium losses. High phosphoric acid intake from soft drinks can theoretically disturb calcium-phosphate balance, though the evidence base is moderate. High caffeine intake (more than 4 cups of coffee daily) slightly reduces calcium absorption.

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