Bone Structure and Physiology

Bone matrix has two main ingredients. The organic part is mostly type I collagen, giving tensile strength and some flexibility, and the inorganic part is a calcium phosphate mineral, hydroxyapatite, giving stiffness and resistance to compression, so bone is both strong and slightly springy rather than brittle.

At the macroscopic level there are two forms. Cortical (compact) bone is dense, forming the outer shell and shafts of long bones and most of the skeleton by mass. Trabecular, or cancellous, bone is the porous, honeycomb-like tissue at the ends of long bones and within the vertebrae, and it is more metabolically active and turns over faster. A typical long bone has a central shaft (the diaphysis), flaring metaphyses and epiphyses at each end, with the growth plate (physis) between them in the growing skeleton, wrapped in periosteum, lined by endosteum, around a central medullary cavity.

Microscopically, cortical bone is organised into osteons, or Haversian systems, which are concentric rings of bone around a central canal carrying vessels and nerves, while trabecular bone is arranged as interconnecting lamellar struts, and osteocytes sit in small spaces within the matrix, connected through tiny channels. Three main cell types keep bone alive. Osteoblasts lay down new matrix, osteocytes are former osteoblasts trapped within it that act as its mechanical sensors, and osteoclasts, large multinucleated cells, resorb bone by dissolving mineral and digesting matrix. They work in a continuous remodelling cycle: osteoclasts resorb a packet of old bone, then osteoblasts form and mineralise new bone in its place. The balance is governed largely by a signalling system in which receptor activator of nuclear factor kappa-B ligand (RANKL) drives osteoclast formation and a decoy, osteoprotegerin (OPG), blocks it.

Bone constantly adapts to mechanical load, the principle behind Wolff's law. Osteocytes sense the strain from weight-bearing and muscle pull and signal for bone to be strengthened where needed, while unloading, from bed rest or spaceflight, causes bone loss. Hormones regulate the mineral side: parathyroid hormone and vitamin D raise calcium availability, calcitonin opposes resorption, and oestrogen restrains turnover, so its loss accelerates bone loss. Most bone mass is accrued by late adolescence or early adulthood, with site-specific consolidation continuing into the third decade, set by genetics, nutrition, loading and hormones, and overall bone strength depends on both this density and the quality of the underlying architecture.

Bone problems reach the SEM clinic in a few recognisable ways. A bone stress injury presents as load-related bony pain that builds over weeks with a change in training, and reflects load outstripping the bone's ability to adapt. Reduced bone strength, from low peak bone mass or later bone loss, may first show as a fragility fracture, one from a force that should not break a healthy bone. In athletes, low energy availability, often with menstrual disturbance, drives bone loss through hormonal and metabolic effects, part of the picture of relative energy deficiency in sport (RED-S). The history, the site and the athlete's wider health together point to the underlying bone problem.

Bone is assessed with imaging, blood tests and bone densitometry. For a suspected bone stress injury a plain radiograph is often first but is frequently normal early, so magnetic resonance imaging is the gold standard when suspicion persists or the site is high risk. Bone mineral density is measured by dual-energy X-ray absorptiometry (DXA): a T-score, against a young adult reference, is used in postmenopausal women and men aged 50 and over, while a Z-score, against age and sex-matched controls, is used in premenopausal women, men under 50 and children. A Z-score of minus two or below is termed below the expected range for age; in a weight-bearing athlete, expected to have above-average density, a value below minus one is already low. Blood tests cover calcium, phosphate, vitamin D, parathyroid hormone and alkaline phosphatase, with hormonal and nutritional tests where relative energy deficiency or another cause is suspected.

Optimising bone health rests first on mechanical loading and nutrition. Weight-bearing, impact and progressive resistance exercise stimulate bone formation, whereas non-weight-bearing activities such as swimming and cycling provide less osteogenic stimulus, which matters for athletes in those sports. Adequate calcium and vitamin D support mineralisation, corrected by diet or supplements where intake or levels are low. In an athlete with low energy availability, restoring energy intake and addressing the wider picture of relative energy deficiency in sport is central, with dietetic and multidisciplinary input. A bone stress injury is managed by its risk: a high-risk site needs protected loading and prompt specialist referral, while a low-risk site needs relative rest and graded loading. Where bone density is low enough to warrant medication, antiresorptive drugs that reduce osteoclast activity, such as bisphosphonates, are considered under specialist guidance, following current UK guidance on osteoporosis.

Rehabilitation after a bone stress injury depends on the site. High-risk injuries, such as the femoral neck, the anterior tibial cortex, the navicular and the base of the fifth metatarsal, can progress to a full fracture or non-union, so they need immediate unloading, prompt specialist referral and a slow, conservative return. Low-risk injuries, such as the posteromedial tibia, the fibula and the lesser metatarsals, can follow a symptom-guided progressive loading programme, often a graded walk-run. In both, loading is reduced to settle symptoms then rebuilt gradually, and training load is monitored as volume and intensity rise. Throughout, energy availability and bone health are addressed, since a bone remodelling under a nutritional or hormonal deficit will not tolerate a rapid return.

• •Weight-bearing impact and resistance exercise build and maintain bone strength, and UK guidance recommends regular impact activity with muscle strengthening for bone health.
• •Non-weight-bearing sports such as swimming and cycling provide less osteogenic stimulus than impact and resistance work, so athletes in these sports may need additional loading.
• •Adequate calcium and vitamin D underpin bone mineralisation and are corrected where deficient.
• •Low energy availability and relative energy deficiency in sport impair bone health, and restoring energy availability is central to recovery.
• •Where fracture risk is high, exercise complements rather than replaces the medication used to strengthen bone.

• •Bone matrix is type I collagen (tensile strength) plus hydroxyapatite mineral (stiffness).
• •Cortical bone forms the dense shell and shafts; trabecular bone is the active tissue at bone ends and in the vertebrae.
• •Osteoblasts build bone, osteoclasts resorb it, and osteocytes sense mechanical load.
• •Bone adapts to load, the basis of Wolff's law, so loading builds bone and unloading loses it.
• •Most bone mass is laid down by late adolescence or early adulthood, consolidating into the third decade.
• •Bone mineral density is measured by dual-energy X-ray absorptiometry, using a Z-score in younger athletes.