Osteoporosis

Osteoporosis is a skeletal disorder of reduced bone mass and deteriorated bone microarchitecture that lowers bone strength and increases the risk of fracture. As an endocrine and metabolic bone disease, it reflects an imbalance in bone remodelling, often driven by oestrogen loss after menopause and by ageing.

Definition

Osteoporosis is a systemic skeletal disease characterised by low bone mass and microarchitectural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture.

Scope

This entry describes osteoporosis as a metabolic bone disorder: how bone strength is lost, the principal risk factors, the burden of fragility fractures, and the biological basis of bone loss. It is a reference overview written from the perspective of mineral and bone metabolism and does not provide individual screening thresholds, drug regimens, or treatment instructions. A separate atlas node addresses osteoporosis from a pathology standpoint.

Core questions

• What makes bone strong, and how is that strength lost in osteoporosis?
• Why does bone loss accelerate after menopause and with ageing?
• How common and costly are osteoporotic fragility fractures?
• What cellular signalling underlies excessive bone resorption?

Key concepts

• Bone mineral density
• Fragility fracture
• Bone remodelling imbalance
• Oestrogen deficiency and bone loss
• RANKL/osteoprotegerin signalling
• Trabecular and cortical bone
• Fracture risk

Mechanisms

Bone strength depends on both the quantity of bone (bone mineral density) and the quality of its microarchitecture. Throughout life bone is remodelled by basic multicellular units in which osteoclasts resorb bone and osteoblasts form it; in osteoporosis resorption outpaces formation, thinning trabeculae and cortices. Oestrogen normally restrains osteoclast activity, so its decline after menopause increases osteoclast number and lifespan, accelerating bone loss. At the molecular level, osteoblast-lineage cells express RANKL to drive osteoclast differentiation and secrete osteoprotegerin as a decoy that restrains it; a shift toward RANKL favours resorption. The net result is reduced bone strength and an increased likelihood that ordinary loads cause fracture.

Clinical relevance

Osteoporosis is clinically important because it predisposes to fragility fractures, especially of the hip, spine, and wrist, which carry substantial morbidity and cost. This entry characterises the disease and its biology as reference material; it is not a guide to who should be screened or how any individual should be treated, and clinical decisions belong to qualified clinicians using current guidelines.

Epidemiology

Osteoporosis and the fragility fractures it causes are common in older populations, particularly postmenopausal women, and impose a large and growing public-health and economic burden; projections for the United States estimated millions of osteoporosis-related fractures annually with rising costs over time (Burge et al., 2007).

Evidence & guidelines

Authoritative narrative reviews summarise the disease and its management framework (Compston et al., 2019; Black & Rosen, 2016). Specific diagnostic thresholds and therapeutic recommendations are set by current society guidelines and are deliberately not reproduced here.

History

Osteoporosis was long understood descriptively as age- and menopause-related bone loss, with bone mineral density measurement later providing an operational way to quantify it. The discovery around 2000 of the RANKL/RANK/osteoprotegerin system gave a molecular explanation for accelerated resorption and reframed osteoporosis as a disorder of remodelling signalling.

Key figures

• Lawrence Riggs
• Sundeep Khosla
• Juliet Compston
• Dennis Black

Seminal works

• compston-2019
• black-2016
• hofbauer-2000

Frequently asked questions

What is the difference between osteoporosis and normal bone ageing?

Some bone loss accompanies normal ageing, but osteoporosis denotes loss severe enough that bone strength is compromised and fractures occur from low-energy trauma; it reflects an imbalance in which bone resorption exceeds formation.

Why are postmenopausal women at particular risk?

Oestrogen restrains bone-resorbing osteoclasts, so the fall in oestrogen after menopause increases osteoclast activity and accelerates bone loss, making postmenopausal women a high-risk group.