Bones, joints and muscles: structure and function

Bone is not built once and then left alone. It is continuously removed and replaced in small packets through a cycle called remodelling, which repairs fatigue damage, adjusts bone strength to the loads actually placed on it, and releases calcium when the blood level falls. The cycle runs in a fixed sequence. Osteocytes detect the mechanical strain and signal for repair. Osteoclasts arrive and resorb a small trench of old bone. Osteoblasts then follow, filling the trench with new bone matrix that is later mineralised. In healthy adults the two phases are coupled, so the amount removed equals the amount replaced.

The coupling is controlled by hormones and by local signals: parathyroid hormone, released when the blood calcium falls, increases bone resorption to release calcium; vitamin D, activated by the kidney, increases calcium and phosphate absorption from the gut so that the raw material for new bone is available; oestrogen restrains resorption, which is why its fall after the menopause tips the balance toward removal; and mechanical loading, from walking or resistance exercise, keeps the osteoblasts active. Two quantitative facts make this clinically concrete. First, about 99 per cent of the body’s calcium is stored in bone, so the skeleton is also the body’s calcium reservoir, and a chronic calcium deficit cannot be corrected without borrowing from it.

Second, because remodelling continues throughout life, the balance is a trend rather than an event: a small excess of resorption sustained over years removes enough bone to cause a fragility fracture. That is exactly what happens in osteoporosis, where osteoclast activity outpaces osteoblasts. Paget’s disease is a different disturbance of the same cycle: the remodelling becomes chaotic and overactive, producing bone that is dense but disorganised and weak. The nursing relevance lies in what can be changed: weight-bearing activity and adequate calcium and vitamin D support the building side, and medicines such as bisphosphonates act by damping the resorbing side, so patient education about taking them correctly is a direct intervention on the balance.

Bone forms in two different ways depending on what it has to become. Flat bones such as those of the skull develop directly within a membrane, a process called intramembranous ossification. Most long bones develop instead from a cartilage model that is progressively replaced by bone, a process called endochondral ossification. Growth in length happens at the epiphyseal plate, a layer of cartilage near each end of a growing long bone, where cartilage cells multiply on the epiphyseal side, enlarge as they move towards the shaft, and are then replaced by bone. Because the plate is the weakest part of a growing bone, it is the site of the injuries and infections that matter in children.

A growth plate injury can stop lengthening on one side only, producing a limb-length difference or an angular deformity, which is why any injury near a child’s joint is taken seriously even when the X-ray looks minor. Growth in width works differently: osteoblasts on the outer surface of the periosteum lay down new bone all around the shaft, while osteoclasts on the inner surface remove bone, so the shaft widens and its wall thickens without becoming solid. This explains several familiar findings. Growth stops when the epiphyseal plates close, which is why adult height is fixed and why the timing of puberty matters for final height.

It also explains why a child’s bone bends and cracks on one side rather than snapping like an adult’s: a child’s bone is more porous and its periosteum is thicker and stronger, so a greenstick fracture, in which one side breaks and the other bends, is common in children and rare in adults. The same thick periosteum is why children’s fractures often heal quickly — the blood supply is generous and the surrounding sleeve of tissue helps hold the fragments. Finally, it explains achondroplasia, the most common cause of disproportionate short stature: the mutation affects cartilage growth, so the long bones of the limbs do not lengthen normally while the trunk and head are less affected.

A synovial joint is a small machine with several parts, and the clinical picture of an arthritis depends on which part is attacked. Articular cartilage covers the bone ends. It has almost no blood supply and very little capacity to repair, and it distributes load and allows near-frictionless gliding. The synovial membrane lines the capsule and secretes synovial fluid, a viscous lubricant that also nourishes the cartilage. The fibrous capsule and its ligaments limit unwanted movement. Bursae are small fluid-filled sacs near the joint that cushion tendons as they glide. Muscles crossing the joint provide active stability and movement. Read each common arthritis against that list.

In osteoarthritis, the failure begins in the cartilage: years of load, injury or inherited tendency erode the surface, the joint space narrows on X-ray, the bone ends thicken and the patient has pain that is worse with use and better with rest. In rheumatoid arthritis, the failure begins in the synovial membrane: an autoimmune process makes the synovium inflamed and thickened, it invades and destroys cartilage and bone, and the pattern is different — symmetrical small joints, morning stiffness lasting more than an hour, and general symptoms such as fatigue, because the disease is systemic and can also affect the heart, lungs, nerves, eyes and skin.

In septic arthritis, the joint is invaded by organisms, so the picture is acute, hot, swollen and extremely painful, and it is a medical emergency because enzymes from the organisms and from the immune response destroy cartilage within days. In gout, the failure is metabolic: uric acid crystals deposit in the joint and trigger an intense inflammatory attack, classically in the first toe joint, with redness, warmth and exquisite tenderness. Recognising which tissue is failing explains why the treatments differ: analgesia and load reduction for osteoarthritis, disease-modifying drugs that suppress the immune attack in rheumatoid arthritis, urgent antibiotics and drainage in septic arthritis, and anti-inflammatory treatment plus urate lowering in gout. The nurse who understands the tissue can also explain the treatment to the patient, which is what makes adherence possible in the long, slow arthritides.