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5.9 — Fractures, Osteoporosis and Arthritis
Bone is the only tissue in the body that heals by regeneration rather than scarring. A cut in skin heals with a scar that is permanently different from the surrounding tissue. A healed fracture, given time, becomes indistinguishable from bone that was never broken — the callus is remodelled away entirely, and after a year or two even an X-ray may show nothing.
That is remarkable, and it explains most of how fractures are treated: the surgeon's job is mainly to hold the pieces in an acceptable position and let the bone do the rest.
How a fracture heals
Stage 1: haematoma, hours to days. The fracture tears blood vessels in the bone and periosteum, and a clot forms between and around the fragments. Bone cells at the fracture edges die from loss of blood supply. Inflammatory cells arrive, clear debris, and release the signals that start everything else.
Stage 2: soft callus, days 5 to 21. Fibrous tissue and cartilage bridge the gap, forming a soft collar around the fracture. The fracture is no longer mobile but is far too weak to bear load. This is why the first three weeks matter most for immobilisation.
Stage 3: hard callus, weeks 3 to 12. The cartilage is replaced by woven bone — disorganised, laid down quickly, mechanically inferior to normal bone but much stronger than cartilage. On X-ray this is when the fracture line starts to disappear and a visible bulge appears around it. The bone is now clinically united.
Stage 4: remodelling, months to years. Osteoclasts and osteoblasts reshape the woven bone into properly organised lamellar bone, aligned to the loads the bone actually experiences (Wolff's law, Chapter 5.1). The bulge is removed. In children this can straighten quite substantial angulation.
Typical times to union: 3 to 4 weeks for a child's forearm, 6 to 8 weeks for an adult's wrist, 12 to 16 weeks for a tibia, and considerably longer for the femoral neck. Children heal roughly twice as fast as adults and remodel far better, which is why angulation that would need correcting in an adult can be accepted in a child.
What stops a fracture healing
Movement. Some micromovement actually stimulates healing; too much prevents the soft callus organising. This is why fractures are immobilised, and why a plate must be rigid enough.
Poor blood supply. The scaphoid, the femoral neck and the talus are the classic problem sites, all for the same reason (Chapters 5.5, 5.6, 5.7).
Infection. Bone infection — osteomyelitis — is notoriously hard to clear, because antibiotics penetrate poorly into dead bone and biofilm.
Gap. If soft tissue is caught between the fragments, they cannot bridge.
Smoking. This one is worth stating plainly because patients are rarely told how large the effect is. Smoking roughly doubles the time to union and substantially raises the rate of non-union. Nicotine constricts blood vessels and carbon monoxide reduces oxygen delivery, and bone healing is highly oxygen-dependent. Stopping smoking during fracture healing has a bigger effect than most drugs available.
Certain drugs. Long-term steroids impair healing. Anti-inflammatory drugs may slow it, though the clinical significance is debated. Chemotherapy delays it.
Diabetes and malnutrition both impair it.
Non-union — no healing after the expected time — is treated by bone grafting, better fixation, or stimulation techniques.
Malunion — healed in the wrong position.
Fracture patterns and what each tells you
Transverse — straight across. Caused by a direct blow. Oblique — angled. From a bending force. Spiral — winding around the shaft. From a twisting force, and this matters in child protection: a spiral fracture of the femur in a child too young to walk is a strong indicator of non-accidental injury, because a child who cannot generate that twisting force cannot cause it themselves. Comminuted — three or more fragments. High energy. Greenstick — the bone bends and cracks on one side only, like a green twig. Children only, because their bones are more flexible and their periosteum is thicker and holds the fracture together. Torus (buckle) — the cortex crumples on the compression side. Children only, and it heals fast. Avulsion — a tendon or ligament pulls a fragment of bone off. Pathological — through bone weakened by disease. A fracture from a trivial force should always raise the question of what weakened the bone — a tumour, a metastasis, a cyst or osteoporosis. Stress fracture — accumulated microdamage outrunning repair (Chapter 5.1). Common in runners and military recruits, in the tibia and metatarsals, and often invisible on early X-rays, needing MRI or a repeat film two weeks later.
Open (compound) fracture — the bone has broken the skin. This changes everything: it is contaminated, and the risk of osteomyelitis is high. Treatment is antibiotics within an hour, tetanus cover, and surgical washout urgently, and the wound is not simply closed.
The two complications that must not be missed:
Compartment syndrome. Muscles are enclosed in compartments bounded by tough fascia that cannot stretch. Bleeding or swelling inside a compartment raises the pressure until it exceeds capillary pressure, and the muscle and nerve inside die from lack of blood supply while the main artery is still open and the pulse is still present.
This is why "the pulse is fine" is not reassurance. The signs are pain out of proportion to the injury, pain on passive stretching of the muscles in that compartment, and a tense swollen compartment. Numbness follows. A missing pulse is a very late sign and by then the muscle is already dead.
Treatment is fasciotomy — surgically splitting the fascia — within hours. Delay causes permanent contracture and sometimes amputation. A cast that feels too tight, in a patient with increasing pain, is split or removed without waiting, and no one is ever criticised for splitting a cast unnecessarily.
Fat embolism. Fat from the marrow enters the circulation, typically 24 to 72 hours after a long bone fracture. The triad is breathlessness, confusion, and a petechial rash across the chest, neck and armpits. Supportive treatment, and early fixation of the fracture reduces the risk.
Osteoporosis
Osteoporosis is loss of bone mass with normal mineralisation — there is less bone, but what remains is chemically normal. Osteomalacia is the opposite: normal quantity, poor mineralisation, from vitamin D deficiency. They are often confused, and the distinction changes the treatment completely.
Bone mass peaks at around age 25 to 30, then declines. In women, the decline accelerates sharply after menopause, with 2 to 3 percent lost per year for about five to ten years, because oestrogen restrains osteoclasts and its withdrawal releases them.
The scale: roughly 1 in 3 women and 1 in 5 men over 50 will have an osteoporotic fracture. Worldwide, an osteoporotic fracture occurs about every three seconds.
Diagnosis is by DEXA scan, which reports a T-score: how many standard deviations your bone density is from a healthy young adult's.
- T-score above −1.0: normal
- −1.0 to −2.5: osteopenia
- Below −2.5: osteoporosis
- Below −2.5 with a fracture: severe osteoporosis
But the T-score alone should not decide treatment. Fracture risk depends on falls, age, previous fracture, steroid use, smoking, alcohol and family history as much as on density. Risk calculators such as FRAX combine these into a ten-year fracture probability, and treatment thresholds are set on that rather than on the scan number alone. A 75-year-old with osteopenia and a previous fracture may be at higher risk than a 55-year-old with osteoporosis and none.
Vertebral fractures are the commonest and the most underdiagnosed. Around two thirds cause no acute symptoms at all — they present as progressive height loss and increasing thoracic kyphosis. Losing more than about 4 centimetres of height is a reason to investigate.
Treatment
Everyone: calcium 1,000 to 1,200 mg daily, preferably from diet, and vitamin D 800 to 1,000 IU daily. Weight-bearing and resistance exercise. Stopping smoking. Limiting alcohol. And fall prevention, which is frequently the highest-yield intervention of all — reviewing medications that cause dizziness, checking vision, removing rugs, and balance training.
Bisphosphonates (alendronate, risedronate, zoledronic acid) are first-line. They bind to bone mineral and are taken up by osteoclasts, which then cannot function — so they reduce bone resorption and let the slower formation catch up. They reduce vertebral fractures by around 40 to 70 percent and hip fractures by around 40 percent.
They must be taken correctly or they do not work and cause harm. Oral bisphosphonates are absorbed extremely poorly — less than 1 percent — and food blocks it entirely. They are taken first thing in the morning with a full glass of plain water, and the person must remain upright and take nothing else for 30 to 60 minutes, because the tablet can cause severe oesophageal ulceration if it lodges.
Two rare but real side effects get disproportionate attention and should be stated accurately. Osteonecrosis of the jaw occurs in roughly 1 in 10,000 to 1 in 100,000 patient-years on oral treatment for osteoporosis — much higher in cancer patients on high-dose intravenous treatment. Atypical femoral fracture is similarly rare. Both are far less common than the fractures prevented, and fear of them has led to substantial undertreatment of people at genuine risk. Drug holidays after 3 to 5 years are used to reduce them.
Denosumab is an antibody that blocks the signal osteoclasts need to form. Given by injection every six months, and effective. Its critical property is that the effect reverses fast on stopping — and stopping without switching to a bisphosphonate causes a rebound with multiple vertebral fractures. This drug must not simply be discontinued.
Teriparatide and abaloparatide are parathyroid hormone analogues, and they are the interesting case. Chapter 5.1 said PTH dissolves bone — and it does, when continuously elevated. Given in a once-daily pulse, it stimulates bone formation instead. The same molecule builds or destroys depending entirely on the pattern of exposure. These are the only widely available treatments that build new bone rather than preventing loss, and they are reserved for severe cases.
Romosozumab blocks a protein that inhibits bone formation, and both builds bone and reduces resorption.
Hormone replacement therapy prevents osteoporosis effectively, and is used where menopausal symptoms are also being treated rather than for bone alone.
Osteoarthritis and rheumatoid arthritis
These two are confused constantly, including by patients who have one and read about the other. They are entirely different diseases with different causes, different distributions and completely different treatments.
| Osteoarthritis | Rheumatoid arthritis | |
|---|---|---|
| Nature | Wear and failed repair | Autoimmune |
| Onset age | Usually over 50 | Often 30–50 |
| Joints | Weight-bearing, thumb base, end finger joints | Hands and feet, middle and knuckle joints |
| Pattern | Asymmetric | Symmetric |
| Stiffness | Under 30 min, after rest | Over 60 min, worst in the morning |
| Pain pattern | Worse with use | Better with use |
| Systemic features | None | Fatigue, fever, weight loss |
| Blood tests | Normal | Raised inflammatory markers, autoantibodies |
| Disease-modifying drugs | None available | Highly effective |
The morning stiffness duration is the single most useful question, and it takes ten seconds to ask. Over an hour points to inflammation; under half an hour points to wear.
Osteoarthritis
Not simply "wear and tear", though that is the shorthand. It is a failure of the balance between cartilage damage and repair, involving the whole joint — cartilage thins and fissures, the bone underneath thickens and forms spurs (osteophytes), the synovium becomes mildly inflamed, and the joint space narrows.
Risk factors: age, obesity, previous joint injury, repetitive loading, and genetics. Obesity is the largest modifiable one, and its effect on the knee is not only mechanical — obesity raises the risk of hand osteoarthritis too, which no amount of loading explains, and adipose tissue's inflammatory signalling (Chapter 4.2) is the likely reason.
Treatment. Exercise and weight loss are the most effective interventions available, and both are consistently underprescribed relative to painkillers. Every kilogram lost reduces knee load by roughly four kilograms per step. Strengthening the muscles around a joint reduces pain measurably.
Then paracetamol (modest effect), topical anti-inflammatories (good effect for knee and hand, few systemic side effects), oral anti-inflammatories (effective, with gastrointestinal, kidney and cardiovascular risks), and steroid injections (useful for a few weeks, and repeated injections may accelerate cartilage loss).
Joint replacement is one of the most successful operations in all of surgery. Around 90 to 95 percent of hip and knee replacements are still functioning at 15 years, and hip replacement in particular produces one of the largest measured improvements in quality of life of any medical intervention.
Rheumatoid arthritis
An autoimmune disease in which the synovial membrane is attacked, thickens into an invasive tissue called pannus, and destroys cartilage and bone from within the joint (Chapter 21.5).
It is systemic, not just articular: fatigue, low-grade fever, weight loss, and involvement of lungs, eyes, blood vessels and heart. Cardiovascular disease is the leading cause of death in rheumatoid arthritis, from chronic inflammation accelerating atherosclerosis — which is why treating the inflammation matters for more than the joints.
And the treatment has been transformed. Before the 1990s, rheumatoid arthritis reliably produced the deformed hands seen in old textbooks. Now, early aggressive treatment with methotrexate and, where needed, biologic drugs prevents most joint destruction, and those deformities have become uncommon in countries with access to treatment.
The critical principle is the window of opportunity. Treatment started within the first three to six months produces substantially better long-term outcomes than the same treatment started a year later, because destruction that has happened cannot be reversed. This is why any patient with persistent symmetrical small joint swelling and prolonged morning stiffness should be referred to rheumatology promptly rather than watched, and it is one of the clearest examples in medicine of a diagnosis where speed changes the outcome permanently.
What Part 6 does next
Bones are levers and joints are pivots. Neither generates any force. Part 6 covers what does: muscle — how a protein filament sliding over another produces movement, how a nerve impulse becomes a contraction, what each major muscle group does, and what happens when the machinery fails.