Osteoarthritis & Rheumatological Bone Disease
This chapter looks like two unrelated subjects joined by an accident of syllabus: arthritis on one side and metabolic bone disease on the other.
They are joined by a single habit of thought. In both, the diagnosis is reached by pattern before it is reached by test.
For a painful joint, the pattern is distribution. Which joints, how symmetrical, whether the spine and entheses are involved, and whether the distal interphalangeal joints are spared. Distribution names the process, and the process is always one of four: mechanical failure, autoimmune synovitis, crystal deposition or entheseal inflammation.
For a diseased bone, the pattern is biochemistry. Calcium, phosphate, alkaline phosphatase and parathyroid hormone together separate the three ways a skeleton can go wrong.
Osteoporosis is too little normal bone. Osteomalacia is a normal quantity of poorly mineralised bone. Paget disease is too much disorganised bone. Hold those three sentences and the metabolic table stops needing memorisation.
1. Osteoarthritis Is Not Wear and Tear
The phrase "wear and tear" is actively misleading, because it implies a passive process in which cartilage simply abrades away with use.
What actually happens is an active, cell-driven remodelling response that has gone wrong. Chondrocytes exposed to abnormal mechanical load upregulate matrix metalloproteinases and aggrecanases, which degrade the very matrix the chondrocytes are meant to maintain.
Low-grade synovial inflammation follows, with cytokine release that amplifies the process. The subchondral bone remodels and stiffens, which further raises the load on the cartilage above it.
Two consequences follow directly and are examinable. Exercise does not accelerate osteoarthritis, and rest does not protect the joint. And osteoarthritis is a disease of the whole joint organ, including bone, synovium, ligament and periarticular muscle, not of cartilage alone.
Reading the radiograph
Four features appear, conveniently recalled as loss of joint space, osteophytes, subchondral sclerosis and subchondral cysts.
The narrowing is asymmetrical, worst where the load is highest, which is the medial compartment of the knee in most Indian patients and the superolateral hip. That asymmetry is the single most useful discriminator from inflammatory arthritis, which narrows the joint uniformly because the pannus attacks the whole surface.
Kellgren and Lawrence grade it from 0 to 4, with grade 4 showing marked narrowing, large osteophytes and definite deformity.
Radiographic severity and symptoms correlate poorly. A patient with a grade 4 knee may walk comfortably while another with grade 2 is disabled, and that mismatch is why the decision to replace a joint is clinical rather than radiological.
Distribution in the hand
Osteoarthritis involves the distal interphalangeal joints, producing Heberden nodes, the proximal interphalangeal joints, producing Bouchard nodes, and the first carpometacarpal joint at the thumb base.
Rheumatoid arthritis characteristically spares the distal interphalangeal joints. A patient with knobbly distal joints and a normal wrist is far more likely to have osteoarthritis than rheumatoid disease.
2. Managing Osteoarthritis
Every major guideline places the same three interventions first: structured exercise, weight reduction and education. They are not preliminaries before the real treatment.
Exercise works through quadriceps strength, proprioception and load distribution rather than through cartilage, which is why it helps even when the radiograph does not change.
| Intervention | Standing |
|---|---|
| Exercise, weight loss, education | First line in every guideline |
| Topical NSAIDs | Preferred over oral for knee, especially in older patients |
| Oral NSAIDs | Effective, limited by gastric, renal and cardiovascular risk |
| Intra-articular corticosteroid | Conditional, useful for 4 to 6 weeks only |
| Intra-articular hyaluronic acid | Conflicting evidence, not recommended by several guidelines |
| Glucosamine and chondroitin | Not recommended |
| Arthroscopic lavage and debridement | Not indicated for degenerative disease |
| Joint replacement | End-stage disease with failed conservative treatment |
Two of these rows are worth knowing precisely because they contradict common practice.
Arthroscopic washout for osteoarthritis, including for a degenerative meniscal tear found incidentally, does not outperform sham or physiotherapy. It remains widely performed and is a recurring examination point.
Intra-articular corticosteroid buys weeks, not months. It is a reasonable bridge to an event or to the start of a rehabilitation programme, not a maintenance therapy.
Osteoarthritis of the knee is disproportionately common in India, and the usual explanations are floor-level activity involving deep squatting and cross-legged sitting, and a high prevalence of obesity in women beyond middle age.
3. Rheumatoid Arthritis
Rheumatoid arthritis is a synovial disease. The synovium proliferates into an invasive mass called pannus, which erodes cartilage and bone at the joint margin.
The erosions are marginal because the bare area, where synovium contacts bone directly without intervening cartilage, sits at the joint edge. That single anatomical fact explains the radiographic signature.
The pattern
Symmetrical polyarthritis of small joints, particularly metacarpophalangeal and proximal interphalangeal joints and the wrists, with the distal interphalangeal joints spared. Morning stiffness lasts more than an hour and improves with use, the opposite of osteoarthritis.
Radiographs show uniform joint space narrowing, periarticular osteopenia and marginal erosions, without the osteophytes and sclerosis of osteoarthritis.
Deformities follow tendon and ligament failure: ulnar deviation at the metacarpophalangeal joints, swan neck and boutonniere deformities of the fingers, and the Z-thumb.
The two facts an orthopaedic or anaesthetic examiner wants
Atlantoaxial subluxation from erosion of the transverse ligament and the odontoid peg is a real hazard in long-standing disease. It may be asymptomatic until the neck is manipulated for intubation, so cervical spine imaging is considered before general anaesthesia.
Anti-cyclic citrullinated peptide antibody is more specific than rheumatoid factor, which also appears in hepatitis C, Sjogren syndrome, endocarditis and healthy older people. Anti-CCP is the better confirmatory test and carries prognostic weight for erosive disease.
Treatment is treat-to-target with disease-modifying drugs, methotrexate first, escalating to biologics if targets are not met. Orthopaedic surgery in modern practice is largely reconstructive for damage already done rather than the mainstay it once was.
4. Seronegative Spondyloarthropathies
The unifying lesion here is not synovitis but enthesitis, inflammation where tendon, ligament or capsule inserts into bone.
That is why the pattern differs so completely: axial involvement, sacroiliitis, dactylitis producing a sausage digit, heel pain at the Achilles and plantar insertions, and a strong association with HLA-B27.
| Condition | Distinguishing features |
|---|---|
| Ankylosing spondylitis | Inflammatory back pain, sacroiliitis, bamboo spine, anterior uveitis |
| Psoriatic arthritis | Skin and nail disease, distal interphalangeal involvement, pencil-in-cup erosion, arthritis mutilans |
| Reactive arthritis | Follows gastrointestinal or genitourinary infection, with conjunctivitis and urethritis |
| Enteropathic arthritis | Accompanies inflammatory bowel disease |
Ankylosing spondylitis
Inflammatory back pain is the opposite of mechanical back pain: worse with rest, worse at night, better with movement, with morning stiffness over 30 minutes and a good response to NSAIDs.
Sacroiliitis is the earliest radiographic change. Later, ossification of the outer annulus produces syndesmophytes, which run vertically and eventually bridge into the bamboo spine, in contrast to the horizontal osteophytes of degenerative disease.
Examination uses the modified Schober test for lumbar flexion and chest expansion for costovertebral involvement. A rigid ankylosed spine fractures easily and unstably, so any spinal pain after minor trauma in these patients needs imaging.
Management is exercise and physiotherapy with NSAIDs as first-line drugs. Conventional synthetic DMARDs do not work for axial disease, though sulfasalazine or methotrexate may help peripheral arthritis.
If disease activity remains high after two NSAIDs, current recommendations move to a biologic, either a tumour necrosis factor inhibitor or an interleukin-17 inhibitor, with Janus kinase inhibitors as targeted synthetic options.
5. Crystal Arthropathies
The two crystals are separated at the microscope, and the distinction is a reliable examination question.
| Feature | Gout | Pseudogout |
|---|---|---|
| Crystal | Monosodium urate | Calcium pyrophosphate dihydrate |
| Shape | Needle | Rhomboid |
| Birefringence | Negative | Positive |
| Classic joint | First metatarsophalangeal | Knee, wrist |
| Radiographic clue | Punched-out erosion with overhanging edge | Chondrocalcinosis |
Managing gout
Acute attacks are treated with NSAIDs, colchicine or corticosteroid, chosen by comorbidity rather than by efficacy.
Urate-lowering therapy is where the marks are. Allopurinol is first-line, including in chronic kidney disease stage 3 or worse, started low at 100 mg daily or less and titrated upward.
The strategy is treat-to-target: titrate against serial serum urate to a target below 6 mg/dL, which reduces flares and improves adherence. Dosing by symptoms alone is the commonest reason therapy fails.
Febuxostat carries a cardiovascular caution. The CARES trial found higher cardiovascular and all-cause mortality than allopurinol in patients with established cardiovascular disease, so it is second-line in that group.
Two prescribing rules complete the picture. Give prophylaxis with colchicine or an NSAID when starting urate-lowering therapy, because the falling urate level mobilises crystals and triggers flares. And never stop urate-lowering therapy during an acute attack in a patient already established on it.
6. The Metabolic Bone Panel
Four numbers separate the metabolic bone diseases, and the table is worth learning as a unit rather than disease by disease.
| Condition | Calcium | Phosphate | Alkaline phosphatase | PTH |
|---|---|---|---|---|
| Osteoporosis | Normal | Normal | Normal | Normal |
| Osteomalacia | Low | Low | High | High |
| Primary hyperparathyroidism | High | Low | High | High |
| Renal osteodystrophy | Low | High | High | High |
| Paget disease | Normal | Normal | Very high | Normal |
Two rows do most of the work in a stem.
Osteoporosis has a completely normal panel. If calcium, phosphate and alkaline phosphatase are abnormal in a patient with fragility fractures, the diagnosis is not simple osteoporosis and something else must be found.
Phosphate separates osteomalacia from primary hyperparathyroidism when both show high calcium demand, and the calcium level separates them decisively: low in osteomalacia because the problem is deficiency, high in hyperparathyroidism because the problem is excess drive.
7. Osteoporosis
Osteoporosis is reduced bone mass with normal mineralisation, and it is silent until something breaks.
Diagnosis is a DXA T-score of −2.5 or lower at the hip or lumbar spine, comparing the patient with a young adult reference. A T-score between −1.0 and −2.5 is osteopenia. The Z-score compares against age-matched peers and is used in younger patients.
A fragility fracture is diagnostic regardless of the DXA result. A fracture from a fall from standing height or less in an adult over 50 defines osteoporosis clinically, and the density measurement then guides treatment rather than establishing the diagnosis.
FRAX estimates ten-year fracture probability from clinical risk factors with or without bone density, which is useful where DXA is not readily available.
The Indian picture
Estimates place roughly 50 million Indians as osteoporotic or with low bone mass, and reported prevalence in Indian women spans a wide range across studies. Vitamin D deficiency is extremely common even in sunny regions, with over half of some studied adult cohorts deficient, reflecting skin pigmentation, covered clothing, indoor work and low dietary calcium.
Indian patients also reach peak bone mass at lower absolute values and present with fragility fractures at younger ages than Western reference populations.
Treatment
Calcium and vitamin D are supportive, not sufficient alone.
Bisphosphonates are first-line antiresorptives. The rare adverse effects worth knowing are osteonecrosis of the jaw and atypical subtrochanteric femoral fracture, both associated with prolonged use, which is the reasoning behind a drug holiday in low-risk patients.
Denosumab, a RANK ligand antibody, is potent but has a critical property: stopping it produces a rebound increase in bone turnover with a risk of multiple vertebral fractures. It must be followed by a bisphosphonate rather than simply discontinued, and doses must be given on time.
Teriparatide is anabolic, working through intermittent parathyroid hormone exposure. Romosozumab inhibits sclerostin and uniquely both builds bone and reduces resorption, with trial data showing substantially lower vertebral fracture rates than placebo.
8. Osteomalacia, Rickets and Paget Disease
Osteomalacia is defective mineralisation of a normal amount of osteoid, almost always from vitamin D deficiency in India. Patients have diffuse bone pain, proximal myopathy with a waddling gait, and difficulty rising from the floor.
The radiographic sign is the Looser zone, a lucent band running perpendicular to the cortex, most often in the pubic rami, femoral neck and scapula. It is a pseudofracture of unmineralised osteoid.
Rickets is the same biochemical failure in a growing skeleton, so the physis is affected. The plate widens because chondrocytes cannot mineralise and continue to pile up, giving cupping and fraying of the metaphysis, the rachitic rosary at the costochondral junctions, and genu varum or valgum once the child bears weight.
Paget disease is excessive, disorganised remodelling. Alkaline phosphatase is very high while calcium and phosphate stay normal, which is the diagnostic signature.
Complications follow from the disorganised bone: pain, bowing of long bones, pathological fracture, deafness from eighth nerve involvement at the skull base, high-output cardiac failure from the hypervascular bone, and sarcomatous transformation in under 1 per cent, which is nonetheless the worst outcome and presents as new pain in a known Paget bone. Bisphosphonates are the treatment.
9. Avascular Necrosis
Avascular necrosis of the femoral head is a bone infarct, and the common causes are worth grouping by mechanism: corticosteroids and alcohol through marrow fat and vascular effects, sickle cell disease through sickling in sinusoids, systemic lupus erythematosus and antiphospholipid syndrome through thrombosis, and caisson disease through nitrogen bubbles.
Radiographs are normal early. MRI is the earliest investigation and detects disease before any radiographic change.
The crescent sign, a subchondral lucency, marks subchondral fracture and is the moment before collapse. Before collapse, core decompression and joint-preserving options are reasonable. After collapse, the joint surface is lost and arthroplasty follows.
10. Worked Examples
Example 1. A 60-year-old woman has painful knobbly swellings of her distal interphalangeal joints and pain at the base of the thumb. Her wrists and metacarpophalangeal joints are normal. Rheumatoid factor is weakly positive. What is the diagnosis?
Osteoarthritis of the hand. The distribution is decisive: distal interphalangeal involvement with Heberden nodes and first carpometacarpal disease, with sparing of the wrist and metacarpophalangeal joints. Rheumatoid arthritis characteristically spares the distal interphalangeal joints and attacks the joints that are normal here. A weakly positive rheumatoid factor is common in older people and lacks specificity; anti-CCP would be the discriminating test if doubt remained.
Example 2. A 68-year-old man with a grade 4 osteoarthritic knee on radiographs walks two kilometres daily without significant pain. Should he be offered a knee replacement?
No. Radiographic grade and symptoms correlate poorly, and the indication for arthroplasty is clinical, meaning pain and functional limitation that have failed exercise, weight management and appropriate analgesia. Operating on a radiograph exposes a comfortable patient to the risks of surgery and to a prosthesis with a finite lifespan.
Example 3. A patient with gout on allopurinol develops an acute attack of the first metatarsophalangeal joint. What should happen to the allopurinol?
It should be continued unchanged. Stopping urate-lowering therapy during a flare causes serum urate to rise again and prolongs the problem, and restarting later triggers a further flare. Treat the attack with an NSAID, colchicine or corticosteroid according to comorbidity. The related rule at initiation is the opposite direction of the same physiology: when starting urate-lowering therapy, give colchicine or NSAID prophylaxis, because falling urate mobilises crystals and provokes attacks.
Example 4. A 55-year-old woman with a vertebral fragility fracture has calcium 7.8 mg/dL, phosphate 2.1 mg/dL, alkaline phosphatase markedly raised and PTH raised. Is this osteoporosis?
No. Osteoporosis has an entirely normal biochemical panel, so an abnormal one means a different or additional diagnosis. Low calcium with low phosphate, high alkaline phosphatase and secondary elevation of parathyroid hormone is the pattern of osteomalacia from vitamin D deficiency. Look for Looser zones on radiographs, proximal myopathy and a waddling gait, and measure 25-hydroxyvitamin D. Treating her with a bisphosphonate alone without correcting the deficiency would be wrong.
Example 5. A 28-year-old man has 8 months of low back pain that is worse in the second half of the night, eases when he gets up and moves, and is accompanied by an hour of morning stiffness. He has had one episode of a painful red eye. What is the diagnosis and how is he treated?
Axial spondyloarthritis, most likely ankylosing spondylitis. The pain is inflammatory rather than mechanical, being worse with rest and better with movement, and anterior uveitis is the characteristic extra-articular association of HLA-B27 disease. Imaging of the sacroiliac joints is the key investigation, with MRI detecting inflammation before radiographic sacroiliitis appears.
Treatment begins with a structured exercise programme and NSAIDs. If disease activity remains high after two adequate NSAID trials, a biologic is indicated, either a tumour necrosis factor inhibitor or an interleukin-17 inhibitor. Conventional DMARDs would be the wrong answer for purely axial disease.
Summary
Distribution names the arthropathy; the calcium, phosphate and alkaline phosphatase panel names the bone disease.
Osteoarthritis is active cell-driven degradation, not passive wear, so exercise helps and rest does not protect.
Radiographic osteoarthritis: asymmetrical narrowing, osteophytes, subchondral sclerosis and cysts.
Osteoarthritis takes the distal interphalangeal joints; rheumatoid arthritis spares them.
Exercise, weight loss and education are first-line in every guideline.
Intra-articular steroid works for 4 to 6 weeks; arthroscopic washout for degenerative disease does not work at all.
Rheumatoid pannus erodes at the bare area, so erosions are marginal.
Check the cervical spine before intubating long-standing rheumatoid disease.
Anti-CCP is more specific than rheumatoid factor.
Spondyloarthropathy is enthesitis: sacroiliitis, dactylitis, heel pain, uveitis, HLA-B27.
Syndesmophytes are vertical; osteophytes are horizontal.
Axial spondyloarthritis: NSAIDs and exercise, then a biologic; conventional DMARDs do not work axially.
Gout crystals are needle-shaped and negatively birefringent; CPPD is rhomboid and positively birefringent.
Allopurinol first-line, titrated to serum urate below 6 mg/dL, continued through flares.
Febuxostat carries a cardiovascular mortality signal in established cardiovascular disease.
Osteoporosis has a normal biochemical panel; a fragility fracture is diagnostic regardless of DXA.
Denosumab must never simply be stopped, because rebound vertebral fractures follow.
Looser zones mean osteomalacia; a very high alkaline phosphatase with normal calcium means Paget disease.
In avascular necrosis, MRI is earliest and the crescent sign marks the moment before collapse.
