Joint types:

  • Synovial (cavitated) – Synovial membranes anchored to capsule, doesn’t cover articular surfaces, numerous villous folds near osseous insertions. Lined by synoviocytes that produce hyaluronic acid, lacks basement membrane hence rapid exchange between blood and synovial fluid. Synovial fluid is filtrate of plasma containing lubracating hyaluronic acid, nourishes hyaline articular cartilage (lacks blood supply). Hyaline cartilage has type 2 collagen, water, proteoglycans, chondrocytes. Cytokines activate degradative enzymes released by chondrocytes, causing matrix breakdown.
  • Nonsynovial (solid, synarthroses) – Lack joint space.
    • Fibrous synarthroses – Cranial sutures, roots of teeth.
    • Cartilaginous synarthroses (synchondroses) – Symphyses (pubic, manubriosternal).

Joint effusions

  • Elbow – Displaced anterior and posterior fat pads.
  • Hip – Displaced fat pads are not accurate. Increased medial joint space.
  • Knee – Suprapatellar to anterior femoral fat pad distance 5-10mm equivocal, >10mm definitive.
  • Shoulder – Massive effusion -> inferiorly displaced humeral head.

Geodes (subchondral cysts) may occur in CPPD, OA, RA, AVN, trauma (can be large, near joints).


  • Alignment – Deformities from ligamentous laxity or damage, erosions, asymmetric cartilage wear.
  • Bone density, new bone formation – Inflammation and hyperaemia induce osteoclasts and resorption; periarticular or regional. Sclerosis from reactive reparitive process eg OA. Enthesophyte is new bone at tendon or ligament insertion eg reactive arthritis, psoriasis, DISH. Syndesmophytes is ossificaion of annular disc fibres.
  • Cartilage – Joint space narrowing from proteolytic enzymes in pannus causing uniform cartilage loss, OA along lines of force, CPPD uniform loss. Preserved in low virulence infection (fungus, TB), amyloid, silastic, gout, early stages of any arthritis, AVN. Ankylosis is fibrous cartilaginous or osseous fusion, following any process completely destrying articular cartilage. Ankylosis distal to wrist most likely trauma, infection or seronegative arthritis.
  • Distribution – Monoarticular, oligoarticular (few joints) or polyarticular. Mono/oligo – in seronegative, infection, PVNS, synovial chondromatosis, crystal or haemophilic arthropathy. Symmetric in RA, CPPD; assymetric in OA, seronegative, gout. Proximal (MCP) disease in RA, crystal; distal (DIP, PIP) in OA; either in seronegative. Spondyloarthropathy involves spine.
  • Erosions – Focal subcortical loss of bone. Marginal erosions at peripheray of joint space in bare areas within joint capsule but not covered by cartilage; active lesions have indistinct edges. Bone proliferation is associated with seronegative arthritis. Nonmarginal usually has sharp sclerotic borders; overhanging edges from reactive bone formation; associated with crystal arthropathies. Subchondral erosions overlap with cysts; due to pannus intrusion in inflammatory disease, liqefactive pressure necrosis or synovial intrusion in noninflammatory disease.
  • Soft tissues – Fusiform swelling centred at joint indicates inflammatory pannus or effusion eg RA, septic arthritis. Diffuse swelling of entire digit suggets more global inflammation (eg enthesitis) in psoriatic and Reiter’s. Eccentric near but not at joints in gouty tophi. Soft tissue calcification from cystals, enthesophytes, vascular, tendons and bursae (dense amorphous hydroxyapatite), CPPD (fine linear deposits in cartilage, capsule, synovium, entheses).

Osteoarthritis (OA)

(Degenerative joint disease, DJD, osteoarthrosis). Chondrocyte injury (aging, genetic and biochemical factors), chondrocyte proliferation and secretion of inflammatory mediators with loss of water and cracking (early OA) then loss of chondrocytes with marked loss of cartilage (late OA). Dislodged pieces of cartilage and subchondral bone form loose bodies (joint mice). Loss of articular cartilage (nonuniform joint space narrowing) causes adaptive bone production including subchondral fibrosis and sclerosis, osteophytes (capped by fibrocartilage and hyaline cartilage that ossify), cortical buttressing, traction enthesophytes (shifts in mechanical loading); less if osteoporosis present. Exposed subchondral bone becomes smooth and polished like ivory (bone eburnation). Subchondral cysts (geode) in weightbearing areas with sclerotic margin (also seen in RA, CPPD, AVN); ?synovial fluid forced into bone through microfractures, or ?from contusion/microfractures -> cyst. Ankylosis is rare unless associated with trauma. Ligament abnormalities with joint deformity (focal cartilage loss). Subchondral bone is less compliant and remaining cartilage subject to greater stress, adaptive remodelling occurs with deformity. Pain with weightbearing, limited ROM, crepitus. Radiographic severity doesn’t always correlate with degree of pain. Heberden nodes from osteophytes at DIPJs (esp women).

  • Primary/idiopathic OA (most) – Aging phenomenon from genearlised ‘wear and tear’, insidious, no apparent initiating cause. Usually oligoarticular, may be generalised. Kness (esp medial compartment) and hands more commonly affected in women, hips in men, also spine, AC joint, feet. Increases exponentially after 50yo, involving 80-90% of those >65yo.
    • Erosive/inflammatory OA (Kellgren arthritis) – Uncommon, primarily middle-aged women with inflammatory episodes, can be painfully debilitating. Additional soft tissue swelling and central erosions esp DIPJs and PIPJs. Gull-wing appearance – proximal margin central erosion and marginal osteophytes. DDx psoriatic arthritis; most of those with OA also have thumb CMCJ and STTJ involvement.
  • Secondary OA (5%) – From trauma (overt or repeditive microtrauma, occupational stresses), abnormal mechanical forces (congenital deformity, meniscal tear, loose bodies, osteochondral fracture), chronic joint disease (haemochromatosis, RA), underlying systemic disease (diabetes, ochronosis, obesity). Usually younger age.

Specific joints:

  • Hands and wrists – Thumb CMCJ, STTJ (schaphoid-trapezium-trapezoid complex), DIPJs, PIPJs, less commonly MCPJs. Radiocarpal or DRUJ involvement almost always secondary to trauma.
  • Shoulder – AC joint common. Glenohumeral joint uncommon except if there is previous trauma or chronic rotator cuff tear/instability. Marginal osteophytes around glenoid, ring osteophytes aroumd anatomic neck of humerus.
  • Hips – Early findings include acetabular subchondral cyst, calcar buttressing (thickened cortex medial femoral neck). Femoral heads migrate superolaterally in 80%, medial/axial in 20% (± protrusio acetabuli). Normal joint space 2-7mm. Ring osteophytes around subcapital femoral neck. Enthesophytes at hip and pelvic apophyses. Later, large inferomedial femoral head osteophytes may simulate flattening of head in old AVN. Rapidly destructive hip disease – unusual variant OA mostly elderly women with rapid femoral head and acetabular destruction similar to infection or Charcot’s joint.
  • Knees – If single-compartment then usually medial with varus deformity and lateral subluxation. Enthesophytes anterior patella esp quadriceps insertion.
  • Sacroiliac joints – Subchondral sclerosis and marginal osteophytes, can be large bridging anteriorly (similar to osteblastic mets).
  • Spinal facet joints – Esp C5-7, L4-S1, may be assymetrical. May cause spondylolisthesis without spondylolysis, foraminal and canal stenosis.
  • Uncinate joints C3-7 – May cause foraminal or canal stenosis.

DDx CPPD, haemochromatosis.

Rheumatoid Arthritis (RA)

Most common purely erosive inflammatory arthropathy. F:M 2-3:1, first develops young/middle-aged adult, 1% of population. Chronic systemic connective tissue disorder, from exposure of a genetically susceptible host to an arthritogenic antigen leading to an autoimmune reaction affecting multiple tissues. 80% have autoantibodies to the Fc portion of IgG (rheumatoid factor RF), not specific, falsely positive in older patients. Many have antibodies to cyclic citrulline-modified peptides (anti-CCP) with high specificity. Affects synovial joint with synovial oedema, hyperplasia, inflammation, hypervascularity with superficial haemosiderin deposits. Organising fibrin may float in the joint space as rice bodies which may calcify. Underlying bony osteoclastic activity allows synovium to penetrate bone causing juxta-articular erosions. Pannus is mass of synovium and stroma with inflammation, granulation tissue and fibroblasts; once cartilage has been destroyed may bridge apposing bones to form fibrous ankylosis which eventually ossifies. Continuous or episodic joint symptoms including early morning stiffness, pain, boggy swelling, tendon contractures and ruptures, deformities. Tx corticosteroids, DMARDs (eg methotrexate), anti-TNF (increases risk of infections esp TB).

Variable appearances. Fusiform soft tissue swelling (effusion and synovitis), periarticular osteoporosis early in disease (from hyperaemia then later disuse), uniform joint space narrowing (cartilage destruction, marked in large joints), marginal erosions (very early dot-dash pattern of articular cortex; initially marginal then subchondral when cartilage destroyed; esp small indistensible joints of hands/feet), polyarticular (axial and appendicular skeleton, large and small joints), bilaterally symmetric. Longstanding may -> superimposed OA (but reduced sclerosis and osteophytosis). Any bone production, periostitis, enthesopathy, osteophytes are unusual (unless there is secondary OA, except distal ulna in minority of long-term RA = ulnar capping), akylosis very rare (except fibrous carpal and tarsal ankylosis).

  • Hands and wrists – Proximal involving DRUJ, pisotriquetral (best seen on Norgaard views), ulnar styloid, radial styloid, scaphoid waist; then midcarpus, CMCJs, MCPs; then PIPJ, DIPJs (when diffuse disease). Ulnar capping productive bone. Ligament rupture may -> ulnar translocation (entire carpus moves), scapholunate dissociation, DRUJ subluxation/dislocation, VISI and DISI. Tendon rupture may -> MCP ulnar deviation volar subluxation/dislocation, swan neck deformities (PIPJ hyperextension, DIPJ hyperflexion), Boutoniere deformities (PIPJ hyperflexion, DIPJ hyperextension), Hitchhiker’s thumb (MCPJ flexion, IP extension).
  • Elbow – Common, synovitis and/or effusion, olecranon bursitis.
  • Shoulder – AC erosion of distal clavicles and coracoclavicular ligament insertion, tapering to a point and sharply defined (cf hyperparathyroidism widened and irregular). Humeral head erosions adjcent to greater tuberosity at anatomic neck capsular insertion. Frequent rotator cuff tear ± mechanical erosion of medial surgical neck by inferior glenoid (due to elevation of head) which may -> pathological fracture.
  • Feet – Early MTP (esp 5th), lateral IPJs and tarsals. Lateral deviation MTP, hammer toe deformities (flexion PIPJs and DIPJs), cock-up deformities (hyperextended MTPJs). Retrocalcaneal bursitis obliterating pre-Achilles fat triangle ± erosion posterior calcaneus (DDx psoriatic and Rieter’s).
  • Knees – Very common with joint effusion, popliteal/Baker cysts due to increased intra-articular pressure. Valgus deformity. Patellar tendon rupture ± anterior distal femoral mechanical erosion.
  • Hips – Femoral heads migrate axially (cf OA superolaterally) with concentric joint space narrowing. Acetabular remodeling causes protrusio acetabuli deformity (femoral head cortex medial to ilioischial line; also seen in 20% of OA). Decompression of pannus and fluid into the iliopsoas bursa.
  • Spine – Cervical spine affected in 50%. C1/2 atlantoaxial subluxation with pannus around dens causing transverse antlantoaxial ligament laxity or disruption (distance >2.5mm increased in flexion usually not symptomatic until 9mm, abnormal spinolaminar line), reduced canal width. Atlantoaxial impaction from C1/2 erosion and facet collapse, with basilar invagination (protrusion of odontoid peg into foramen magnum, anterior arch atlas at body of axis instead of superior peg), more commonly causes neurological Sx than subluxation. Odontoid erosion, unilateral facet erosion (may -> torticollis), erosions at facets and joints of Luschka, mechanical erosion of spinal processes, ‘discitis’ appearances (?from osteoporosis, posterior ligament laxity with stair-step deformity, endplate irregulatiy, loss of disc height). T/L/SI uncommon, usually mild (SIJ usually asymmetric).
  • Rheumatoid nodules – In 25%, usually subcutaneous in areas subjected to pressure. Contain fibrinoid necrosis and surrounding epithelioid histiocytes. May also occur in tendon sheaths, lungs, spleen, pericardium, myocardium, heart valves, aorta, other viscera.
  • Vasculitis – Medium to small arteries similar to polyarteritis nodosa (except kidneys not affected). May affect small vasa nervorum and digital arteries causing peripheral neuropathy, ulcers, gangrene.
  • Serositis – Tenosynovitis, bursitis, pleural/pericardial effusions.
  • Interstitial pneumonitis

Robust RA – Large subchondral cysts and normal bone density. Distribution same as RA, predominantely erosive. Usually men with maintained normal activity retaining bone density and forcing decompression of fluid into subchondral cysts.

Adult Still’s disease – Intermittent fever, skin rash, pleuritis, pericarditis, lymphadenopathy, hepatosplenomegaly. Carpal disease predominates with pericapitate erosions and ankylosis.

Juvenile Idiopathic Arthritis (JIA)

(Previously juvenile rheumatoid arthritis JRA, juvenile chronic arthritis). Group encompassing all forms of arthritis developing <16yo and persisting for at least 6/52. Unkown aetiology. Compared to adult RA it is typically pauciarticular/oligoarthritis, assymetrical, more systemic disease, larger joints, absent rheumatoid nodules, most seronegative, commonly antinuclear antibody (ANA) positive. Many have sustained disease activity, but only 10% develop serious functional long-term disability. Clinical subsets/complexes include:

  • Systemic arthritis (Still’s disease, 20%) – <5yo, abrupt, remitting, migratory rash, fever, hepatosplenomegaly, serositis, polyarthritis. Mild radiographic findings.
  • Oligoarthritis/pauciarthritis (40%) – </= 4 joints in 1st 6/12, asymmetric, <6yo girls. Seronegative. 1/4 have chronic iridocyclitis.
  • Rheumatoid factor-positive polyarthritis (juvenile-onset adult RA, 5%) – Similar to adult RA, teenage girls
  • Rheumatoid factor-negative polyarthritis (25%) – Similar to oligoarthritis but >4 joints. Most female, any age. Synovitis with adult-type distribution.
  • Enthesitis-associated arthritis – <6yo, most HLA-B27 positive, mostly lower limbs
  • Psoriatic arthritis (juvenile ankylosing spondylitis AS) – M:F 7:1, strongly HLA B27 positive. Extra-axial arthritis, rarely sacroliitis (may be underdiagnosed due to normal wide ill-defined joint) and spondylitis.
  • Undifferentiated arthritis

Thickened synovium and joint effusions with soft tissue swelling. Osteoporosis, late cartilage destruction and erosions, rare subchondral cysts. Periosteal reaction and ankylosis more common than adult RA. Hyperaemia in skeletally immature -> ballooning of joints with epiphyseal and metaphyseal overgrowth/flaring, accelerated bone maturity with premature physeal fusion in involved joints (later shortened limb). Splenomegaly, pleural effusions.

  • Knee – Widened intercondylar notch.
  • Ankle – Valgus ‘tibial-talar tilt’ (DDx ‘sure does hurt to jog: sickle cell, skeletal dysplasia, haemophilia, traumatic physeal injury, JIA).
  • Wrist and hand – Esp carpus/pericapitate, radiocarpal joint may be spared, small square-appearing carpal bones, narrowed intercarpal joint spaces, early ankylosis common (before significant erosive changes).
  • Elbow – Enlarged trochlear notch, radial head, capitellum.
  • Hip – Enlarged femoral head, short neck, coxa valga, protrusio acetabuli, hypoplastic iliac wings, gracile femoral shaft.
  • C-Spine – Prominent atlantoaxial subluxation, odontoid erosions, facet erosions. Ankylosis common, esp facets (?to protect against discovertebral junction abnormality); if before maturation then vertebral body hypoplasia (vertically and AP) causing ‘waisting’ of bodies.

Seronegative Spondyloarthropathies

(HLA-B27 spondyloarthropathies, formerly rheumatoid variants). Most are human leukocyte antigen HLA-B27 positive (but 6% of general population is also positive). Primary a disease involving entheses, may be axial/spine (most), peripheral or enthesis predominant (with different treatments). Mixed productive and erosive arthropathy. Bony ankylosis, bony proliferation.

  • Ankylosing spondyloarthritis (AS, rheumatoid spondylitis, Marie-Strumpell disease, most common) – M:F 4-10:1 (females tend to be milder), onset in adolescence/young adult with back pain, thoracic kyphosis, limited lumbar lordosis. 90% are HLA-B27 positive. Plasma cells and lymphocyte infiltration in subligamentous bone and diskovertebral junction. Especially sacroiliac and apophyseal joints. Enthesopathy of the Sharpey’s fibres creating syndesmophytes. Usually initially SIJ then T/L and L/S junctions, ascending. Calcification of the disk with enchondral ossification. May have dural ectasia. Romanus (shiny corner) sign – oedema at anterior endplate (ALL attachment) +/- erosion, later replaced by focal fatty replacement. Andersson lesion – oedema just under endplate along the disc. Hips involved in 50% (symmetric or asymmetric) with concentric joint narrowing, mild erosions, protrusio acetabuli, ring osteophytes. May also involve glenohumeral joint, symphysis pubis, sternomanubrial, costochondral joints; less commonly knees, ankles, hands, feet. Enthesitis with ossification esp pelvis, calcaneus, patella. Subchondral cysts, periostitis, ligament disruption uncommon. May be associated with amyloidosis, aortic insufficiency, aortitis, uveitis, regional enteritis, UC, upper lung cavitation and fibrosis. Spinal pseudoarthrosis with instability from occult stress fracture nonunion causing reactive sclerosis, wide area of destruction across fractured ankylosed disk.
  • Psoriatic arthritis – In >10% of patients with psoriasis esp 30-50yo, M=F, can predate skin findings in 20%. Types include oligoarthritis, polyarthritis (esp DIPJs), symmetric type (resembling RA), arthritis mutilans, spondyloarthropathy (30-50%). DIPJs of hands and feet usually involved first. Large joints uncommonly involved (ankle, knee, hip, shoulder), almost always concomitant small joints involvement.
  • Arthropathy of IBD (enteropathic arthritis) – Spondyloarthropathy with UC (in 10-15%), less commonly Crohn’s disease and Whipples disease. 1/3 have sacroiliitis identical to AS. Mild peripheral arthralgia. Often HLA-B27 positive.
  • Reactive arthritis (least common) – Reiter syndrome is a form of reactive arthitis with triad of conjunctivitis, nongonococcal urethritis (cervicitis in females) and arthritis (“can’t see, can’t pee, can’t bend the knee”). M>F, 20-40yo, >80% HLA B27 positive, also affects HIV positive. Usually 1-3 weeks posterior genitourinary infection with Chlamydia tracomatis or GIT infection with Salmonella, Shigella, Yersinia, or Campylobacter; ?antigenic similarity with synovial joint; lasting from several months. 50% have recurrent symptoms. Involves feet MTPJs, calcaneus, ankle, knee with upper extremity usually spared. Spondyloarthropathy similar to psoriatic arthritis.

Syndesmophytes are vertical paravertebral ossifications of peripheral annular fibres (cf horizontal osteophyte; difficult with bridging osteophytes). Excludes RA.

  • Marginal syndesphytes (bamboo spine) – AS, from edge/margin of vertebral body -> margin adjacent body, bilaterally symmetric. Osteitis from erosive enthesitis at superior and inferior anterior corners (marrow oedema with high T2 and enhancement) -> reactive slerosis (‘shiny corner’) -> erosion with loss of normal anterior concavity (squared vertebral body) -> fine ossification of annulus fibrosis at discovertebral junction -> ankylosis (bamboo spine) and undulating fusion of facet joints and interspinous enthesophytes (trolley track on AP with 3 continuous vertical lines). Initially bone density normal, then may be marked disuse osteoporosis vunerable to fracture (esp C/T and T/L junctions through disk space and posterior elements). Ankylosing spondylitis ascends the spine continuously. Spinal ligamentous ossification DDx: DISH, AS, severe spondylosis, Vit A toxicity, fluorosis.
  • Nonmarginal syndesmophytes (parasyndesmophytes) – Psoriatic/reactive, asymmetric large/bulky from body away from endplate/margin. Generally starts in T/L junction with skip levels.

Sacroiliitis common New York criteria on XR:, causing loss of cortical definition (more prominent at ilium due to thinner cartilage) -> erosions and joint widening -> sclerosis -> ankylosis of synovial portion (anteroinferior). Bilaterally symmetric (but may initially be asymmetric/unilateral) in ankylosing spondylitis or IBD. Unilateral or bilateral (usually asymmetric but can be symmetric) in psoriatic or reactive arthritis (unilateral/assymetric also seen in OA, infection, gout). Enthesitis in AS and chronic reactive arthritis may fuse SI syndesmosis (posterosuperior); similar to DISH, severe spondylosis, vit A/D toxicity, fluorosis. DDx osteitis condensans. Areas of marrow fat suggest healed inflammation (vs infection). Radiographic New York criteria:

  • Grade 0 – Normal
  • Grade 1- suspected (blurry margins)
  • Grade 2 – minimal (single erosion, small areas of sclerosis)
  • Grade 3 – advanced (distinct sclerosis, multiple erosions, joint widening, partial ankylosis)
  • Grade 4 – total ankylosis

Hands and wrists more commonly involved in psoriatic arthritis. DIPJs, PIPJs, MCPJs; may be asymmetric or symmetric. Tuft resportion or dense bone proliferation (ivory phalanx). Swelling of entire digit from synovitis of digital tendon sheaths (sausage digit) cf fusiform in RA. Nail changes (thickening, pitting, discolouration), 25-60% HLA B27 positive (usually spondyloarthropathy). Proliferative erosions (ill-defined margins with emanating wisps of periostitis). Marginal erosions may progress to severe subchondral erosions with pencil-in-cup deformity and clinical telescoping. Subtle bone excrescences around joint if severe. Periosteal reaction and small enthesophytes. Ankylosis if severe. Arthritis mutilans – severe deformities with resorption of bone, also seen in RA. Wrist involvement not as common as RA. Subchondral cysts uncommon.

Feet more commonly involved in reactive arthritis. IPJ (esp great toe), MTPJ erosive disease. Retrocalcaneal bursitis with erosions of Achilles insertion (similar to RA, reactive arthritis). Enthesitis of plantar aponeurosis with erosions, enthesophytes. Calcaneal heel spur with ill-defined margins (cf well-defined in OA/trauma).


(Sternoclavicular hyperostosis). Synovitis, Acne (propionibacterium acnes), Pustulosis, Hyperostosis and Osteitis. Uncommon spondyloarthropathy. Anterior chest wall osteitis with painful hyperostosis and soft tissue ossification between medial clavicles, anterior upper ribs and manubrium ± fusion. Rarely extra-axial tumour-simulating bone lesions.

Crystal and Depositional Arthropathies


Humans lack uricase for degradation of uric acid (end product of purine metabolism), found in other mammals. Hyperuricaemia (multiple causes including hereditary) present in >10% of Western population, but only 0.5% develop gout with deposition of monosodium urate (MSU) crystals throughout the body (joint cartilage, capsule, synovium, subchondral bone etc). Primary/idiopathic (90%) from overproduction of uric acid (diet, unkonwn or known enzyme defect) or reduced excretion with normal production. Secondary gout (10%) from increased nucleic acid turnover (eg leukaemia, aggressive neoplasm), inborn errors of metabolism, renal disease, hyperparathyroidism, hypoparathyroidism, psoriasis, diuretics. Middle-aged/elderly men, rare <20-30yo, extremely rare in premenopausal women. Increased risk with heavy alcohol, obesity, drugs (thiazides), lead toxicity, FHx (eg X-linked HGPRT gene). Acute arthritis (lasting hours-weeks) from MSU in joint fluid (needle/rod-shaped, negatively birefringent) -> ?unsucessful phagocytosis of crystals by leukocytes -> inflammatory factor release, neutrophilic infiltration with synovial oedema and congestion. Recurrent acute arthritis -> chronic tophaceous gout (after average of 12yrs) with formation of tophi in synovium, fibrosis, pannus, cartilage destruction. 4-6y before radiographically apparant. Tophi (aggregations of urate crystals surrounded by inflammation) occur in articular cartilage, periarticular ligaments, tendons, soft tissues (olecranon, patella bursae, Achilles tendon, earlobes) etc. Gouty nephropathy is MSU deposition in renal medulla, uric acid renal stones. 40% also have CPPD.

Random distribution but tending to lower limb and small joints (esp MTP great toe), mono/oligoarthritis (may be polyarticular similar to RA). Well-defined erosions with sclerotic margins (rarely seen in other arthritis) with over-hanging edges (nonspecific); erosions may be intra-articular/marginal or para-articular/non-marginal (pathognomonic, tend to be under tophi). Eccentric tophi in periarticular soft tissues or bursa, low T1 variable T2 (depending on calcification), usually enhances, may be heterogeneous, only calcifies with renal failure. Little/no osteoporosis, joint spaces preserved until late, occasionally subchondral cysts (can be large). Secondary OA from chondral deposition or recurrent bouts.

Calcium Pyrophosphate Deposition Disease (CPPD)

(Pyrophosphate arthropathy, pseudogout). Calcium pyrophosphate dihydrate (CPPD) crystal deposition in intra- and extra-articular tisues. Crystals are geometrically shaped and are weakly positively birefringent. M=F, >50yo increasing with age (50% >85yo), presentation may resemble acute gout (‘pseudogout’), contiunous acute attacks (pseudo-RA), chronic progressive (pseudo-degenerative joint disease), rapidly destructive (pseudoneuropathic arthropathy) or asymptomatic arthropathy. May be sporadic/idiopathic; hereditary (earlier age with severe OA, eg AD ANHK gene encoding pyrophosphate transport chanel); or secondary from previous joint damage, hyperparathyroidism, haemochromatosis, hypomagnesemia, hypothyroidism, ochronosis, diabetes.

Chondrocalcinosis in hyaline cartilage, fibrocartilage, synovium or joint capsule; esp in knee menisci and hyaline cartilage, TFC, symphysis pubis (virtually diagnostic), lunatotriquetral ligament, acetabular labrum. Uniform crystal deposition in cartilage with uniform destruction -> OA. May rupture and seed into joint, eliciting inflammatory reaction similar to gout. Severe destruction may mimic neuropathic/Charcot joint (pseudo-Charcot joint). Early erosive changes, later sclerosis, osteochondral fragments, osteophytes. ‘OA with a funny distribution’: bilaterally symmetric esp knee (patellofemoral > medial/lateral compatments), wrist (radiocarpal then scapholunate dissociation, scaphoid and distal radial erosions, SLAC), MCPs (2nd and 3rd; IPJs usually spared), shoulder, elbow. Subchondral cysts common and large. Bone density usually normal. Rarely deposition in soft tissues (eg rotator cuff), unable to differentiate CPPD crystals from calcium hydroxyapatite (in calcific tendinitis, but not seen in cartilage).

Haemochromatosis Arthropathy

Iron deposition throughout body tissues -> fibrosis, organ failure. Middle-aged M>F. Primary from increased GI absorption; secondary from blood transfusions, alcoholism, excess ingestion. 50% have arthropathy, similar to CPPD; esp radiocarpal, 2nd-3rd MCPJs, knee (esp patellofemoral). Block/beak-like osteophytes at MCPJs, chondrocalcinosis, prominent subchondral cysts, occasionally erosions.

Wilson’s Disease

(Hepatolenticular degeneration). Autosomal recessive, M slightly > F. Copper accumulation in tissues with degeneration of basal ganglia, hepatic cirrhosis, corneal Kayser-Fleischer rings (brownish-green). Arthropathy rare, late with chondrocalcinosis, cartilage destruction with indistinct/irregular subchondral bone and fragments/ossicles, osteopenia. Wrist and hand (esp MCPs), feet, hip, shoulder, elbow, knee.

Calcium Hydroxyapatite Deposition Disease (HADD)

Unknown cause ?repetitive minor trauma and calcium deposition in necrotic tissue. Middle/older-aged, M=F. Periarticular calcifications (tendon = calcific tendinitis, ligaments, capsule, bursa, occasionally chondrocalcinosis) that are homogeneous, cloud-like, may enlarge or dissapear with time. Usually monoarticular causing inflammation without structural joint abnormality. Shoulder (esp rotator cuff/biceps tendon insertions, subacromial-subdeltoid bursa), hands (MCPJs, IPJs), wrists (esp flexor carpi ulnaris insertion adjacent to pisiform), gluteus maximus insertion. May be painless or very painful, Tx fluoroscopic/US-guided aspiration/fenestration and steroid injection.


(Alcaptonuria). Inherited absent homogentisic acid oxidase with accumulation of homogentisic acid in tissues, M=F. Late arthropathy with dystrophic calcification (hydroxyapatite) in intervetebral disks, cartilages, tendons, ligaments. Osteoporosis, mild degnereative joint disease.


Primary; or secondary from multiple myeloma, long-term haemodialysis, RA, familial Mediterranean fever, chronic infection, spondyloarthropathy, connective tissue disorders. May cause renal failure, organomegaly, pericardial/myocardial disease, pulmonary septal infiltration, GIT submucosal thickening and decreased peristalsis. Deposition in bone/synovium/ligaments/tendons/soft tissues with bulky nodules (esp around wrists, elbows, shoulder with ‘shoulder pad’ sign) superimposed on atrophic muscles; intermediate MR signal. May have chronic joint effusions, large periarticular collections. Intra-articular deposits -> joint space widening then cartilage destruction and narrowing, erosions and subchondral cysts (sharply marginated); esp wrists, elbow, shoudlers (spine, wrist and hands in haemodialysis). Spondyloarthropathy with disk space narrowing, end plate irregularity (DDx discitis, neuropathic joint). DDx RA.

Connective Tissue Disorders

(Collagen vascular diseases). ?Autoimmune multisystem disease with vasculitis, connective tissue involvement, immune complexes and antinuclear antibodies, may be rheumatoid factor positive. Hands – osteoporosis, soft tissue wasting. Usually no erosions.

  • Scleroderma (systemic sclerosis) – Family of conditions with hardening of the skin, may also involve other organs. F:M 3:1, 20s-40s. Diffuse scleroderma involves distal extremities and trunk; limited scleroderma fingers, hands and face. CREST syndrome (common type of limited scleroderma) – skin Calcinosis, Raynauld’s phenomenon, oEsophageal dysmotility, Sclerodactyly, Telangiectasia. Skin changes, distal joint pain/stiffness, proximal myopathy. Oesophageal atrophy and fibrosis -> dysmotility, reflux with strictures, air-fluid levels. Hidebound thickened squared small bowel folds and pseudosacculations. Soft tissue oedema -> taut shiny and atrophic. Sclerodactyly – localised finger/toe skin thickening/tightening with underlying atrophy and tapering. Acro-osteolysis in 80%. Bony resorption at tufts, thumb CMCJ (with radial subluxation, specific for scleroderma), angle of mandible, posterior ribs (esp 3rd-6th), wrist. Calcification in 25% being SC, extra-articular, intra-articular or punctate within the terminal phalynx. Joint abnormalities eventually occur in 50% with cartilage destruction, erosive changes, mild productive bone changes, flexion contractures.
  • Systemic lupus erythematosus (SLE) – F:M 5-10:1, more common in African-Americans, young adults. Constitutional Sx, rash (esp butterfly rash on face), myositis, neurological abnormalities, pulmonary vasculitis, pulmonary fibrosis, pleural effusions, pericarditis, cardiomyopathy, nephritis. Common nonerosive polyarthritis with deformities (ligament laxity). Mild MSK symptoms despite radiographic appearances. Reducible deformities (appearing more severe on Norgaards view when hands not supported by cassete) with ulnar subluxation of MCPJs and thumb CMCJ, flexion/extension doformities IPJs. Streaky/linear/nodular/amorphous SC calcifications in 10%, usually lower limbs. AVN in 1/3 esp femoral head, humeral head, knee ?due to steroids ± vasculitis; but only symptomatic in 8%.
  • Dermatomyositis and polymyositis – Polymyositis proximal muscle weakness/arthralgias predominate; dermatomyositis diffuse erythematous rash. 20s-40s, F>M, but dermatomyositis may be seen in children (severe). Proximal muscle weakness, ternderness, oedema -> contractures, atrophy, intramuscular calcifications (esp sheet-like along fascial/muscle planes being pathognomonic). Most common calcification is nonspecific subcutaneous, may also be periarticular. Radiographic bone/joint abnormalities are rare.
  • Mixed connective tissue disease (MCTD) – Mixed scleroderma, SLE, polymyositis, RA. Arthritis common in hands, feet, wrists.

Septic Arthritis

See Musculoskeletal Infection

Haemophilic Arthropathy

Repeated haemarthrosis, 50% of haemophiliacs develop severe arthropathy. Spontaneous or minimal trauma, typically first occurs before 2yo. Esp large joints in order of knee, elbow, ankle, hip, shoulder. Synovial hyperplasia, chronic inflammation, fibrosis, haemosiderosis. Synovial mass erodes cartilage and subchondral bone with secondary OA. Widened intercondylar/trochlear notch, squared inferior patella, bulbous femoral condyles with flattened surfaces, enlarged radial head, talar tilt (relative undergrowth of lateral tibial epiphysis). Symemtric loss of joint space, periarticular erosions and subchondral cysts. Hyperaemia causes periarticular osteoporosis, epiphyseal enlargement.


Excessive growth hormone in skeletally mature causing tubular bone widening and acral growth. Soft tissue thickening (esp phalanges and heel pad), enlarged sella (pituitary adenoma), prominent facial bones (mandible and occipital protuberance), enlarged excessively pneumatised paranasal sinuses, increased vertebral body and disk heights, posterior vertebral body scalloping, exaggerated thoracic kyphosis, bony proliferation at entheses. Widened phalanges and metacarplas, spade-like terminal tufts, thickened cartilage (widened joint spaces) prone to injury with premature OA.

Lead Arthropathy

Lead bullets lodged in bursae and joint spaces may dissolve in synovial fluid, fragment throughout the joint lining, synovium and cartilage. May cause lead poisoning. Mechanical cartilage damage -> OA.

Diffuse Idiopathic Skeletal Hyperostosis (DISH)

Most middle-aged and elderly, M>F. Most commonly thoracic and cervical spine. Profound ossification of annulus fibrosis, anterior longitudinal ligament (classic flowing mature anterolateral ossification of few mm thick), paravertebral connective tissues. Usually relative preservation of disk height and litte endplate sclerosis. Advanced -> spine immobility at risk of fracture and spinal injury. SIJ typically superior nonarticular bridging calcification with lower articular 2/3 rarely involved. Prominent enthesophytes esp pelvis, calcaneus, anterior patella. Calcified sacrotuberous and sacrospinous ligaments.


  • Ossification of the posterior longitudinal ligament (OPLL) – Predominantly posterior ossification with some bulky anterior osteophytes. Overlaps with DISH. More commonly cervical spine. May cause spinal canal stenosis. Common in Japan, polynesians.
  • Retinoid arthropathy – Retinoic acid for skin diseases causing hyperostoses esp cervical spine anterior and posterior longitudinal ligament calcification.
  • Fluorosis (long-term fluoride intoxication) – Bulky paraspinous ligament calcifications, but diffusely osteopenic and sclerotic bones in patchy/chalky pattern.


Granulomatous deposits lungs, also bones esp hands (rarely other bones). Characteristic lace-like lytic destructive lesions of cortex. Skin nodules. Advanced – soft tissue swelling, bony dissolution.

Neuropathic Arthropathy

(Charcot’s joint). From diabetes, tabes dorsalis in syphilis (rare, slow demyelination of sensory fibres esp proprioception, vibration, touch), syringomyelia, spinal cord injury/paralysis continuing to use affected limb for support, multiple sclerosis, alcoholism, amyloidosis, intra-articular steroids, congenital insensitivity/indifference to pain, Charcot-Marie-Tooth, dysautonomia. ?Initial alteration in sympathetic nerve control of osseous blood flow -> hyperaemia, bone resorption -> neurotraumatic destructive cycle of blunted pain/proprioception, relaxation of supporting muscles with chronic instability, abnormal joint loading. Usually monostotic, may have rapid progression. Pseudo-Charcot joint in CPPD.

Pathognomonic D’s:

  • Early severe cartilage destruction.
  • Dislocation/disorganisation/deformity (initially subluxation) due to ligamentous and muscle laxity.
  • Debris/detritus, clumps of soft tissue calcification/ossification adjacent to joint.
  • Normal bone density.
  • Joint distension with large effusion, may decompress along fascial planes carrying bone debris.

20% purely hypertrophic, 40% primarily atrophic (severe bone resorption with litter debris, sharp transvere margin in metadiaphysis), 40% combined hypertrophic and atrophic. Ankylosis rare.

Specific joints:

  • Ankle and foot (esp diabetes, alcoholism) – Lisfranc’s joint, talonavicular, subtalar, intertarsals.
  • Knee (tabes dorsalis, diabetes, congenital insensitivity/indifference to pain) – Usually at least partly hypertrophic.
  • Shoulder (syringomyelia) – Atrophic when advanced with resorption of most/all of humeral head and neck, simulating surgical resection or chondrosarcoma with bony debris.
  • Spine (diabetes, instrumented spinal trauma in paraplegics) – Disc space narrowing, paraspinal soft tissue mass. DDx discitis which may have paravertebral abscess but doesn’t have vacuum disk, debris, spondylolisthesis, facet involvement.

DDx infection which has sinus tracts, soft tissue abscesses.

Synovial Chondromatosis

Metaplasia of synovium -> cartilagnious nodules which may grow, become loose (‘joint mice’) or reattach to synovium. M>F, 20s-40s. Enchondral calcification in 70% (synovial osteochondromatosis) with round multifaceted bodies of similar size and variable mineralisation, may be lamellated or contain trabeculae. Esp knee, hip, elbow, shoulder. Joint effusion. If trapped between surface may -> pressure erosions, joint destruction, OA. Tumefactive synovial chondromatosis – tightly packed loose bodies, may be mistaken for chondrosarcoma on histology. DDx loose bodies from OA, TB, trauma (tend to be varying sizes, few). Rx complete synovectomy.

Tenosynovial Giant Cell Tumour

Benign neoplasm of synovial lining in joints, tendon sheaths or bursae. Overexpression of a chemoattractant for macrophages with infiltration. 20-50yo, M=F. Prone to haemorrhage with minor trauma causing haemorrhagic effusions. MRI low signal haemosiderin lining synovium on T1 and T2, blooming paramagnetic effect on gradient. Varaible fat, fibrous tissue, blood, oedema. Tx resection, common recurrence in diffuse type.

  • Diffuse type (previously pigmented villonodular synovitis PVNS ) – Usually monoarticular, may involve more than one joint with pain, locking, swelling. Lobulated red-brown synovial mass with finger-like projections/fronds spreading along surface and infiltrating subsynovial tissue and/or nodules (may be attached to synovium by a pedicle). 80% in knee, others include hip, ankle, calcaneocuboid joint, elbow. Early erosions -> large erosions, occasionally large subchondral cysts. Bone density and cartilage preserved until late. Doesn’t (very rarely) calcifies. Radiographically identical to noncalcified synovial chondromatosis.
  • Localised type (giant cell tumour of tendon sheath) – Painless, slow growing, usually discrete well circumscribed nodule resembling a walnut attached to tendon sheath. Typically finger or wrist, usually not centred on a joint. 15% have adjacent bony erosion/scalloping. Haemorrhage less common than diffuse type.

Reflex Sympathetic Dystrophy (RSD)

(Sudeck atrophy, shoulder-hand syndrome). Minor trauma to extremity -> pain, swelling, dysfuction. Severe, patchy osteoporosis and soft tissue swelling. Usually distal extremity. Pain and swelling subsides, osteoporosis persists, skin may become atrophic.


(Ischaemic necrosis). Avascular necrosis (AVN) is end-stage osteonecrosis. Idiopathic; or secondary to steroids (Cushings or exogenous, ?due to increased size of marrow fat cells hence pressure esp femoral head), trauma (esp femoral head, proximal scaphoid, humeral anatomical head, talar body and dome), aspirin, bisphosphonates, collagen vascular disease/SLE (humeral head, talus), alcohol, idiopathic, renal transplant, sickle cell (humeral head, talus), pancreatitis, infection, caisson disease (dysbaric AVN, nitrogen emboli from rapid decompression), Gaucher’s disease, radiotherapy. Marrow elements die after 6-12/24, osteocytes/osteoblasts/osteoclasts after 12-48/24 and marrow fat cells after 2-5/7 of anoxia. Creeping substitution: necrosis -> revascularisation and granulation tissue with bone resorption along reactive interface (weaker) -> osteoblastic reinforcement -> normal bone. Articular cartilage and cortex is usually unaffected due to collateral blood flow and nourishment by synovial fluid.

Joint effusion -> patchy/mottled relative then true sclerosis (surrounding osteopenia due to hyperaemia then reactive interface; can involve entire condyle/head usually central; 1st radiographic sign at weeks-months) -> thin subchondral lucency/microfractures (cresent sign, not sensitive, from osteoporosis and bone weakening) -> collapse of articular surface and joint fragmentation, flattening, deformity -> severe secondary osteoarthritis. Only occurs on one side of a joint. Increased bone density or subchondral cysts/geodes in otherwise normal joint. MRI most sensitive with early nonspecific marrow oedema then double-line sign (interface between resorption and healing) of serpigenous low (sclerotic bone) with adjacent high (hyperaemic tissue) T2 (DDx straight/smoothly curved subchondral fracture) due to geographic medullary infarcts. Usually anterosuperior femoral head; posterior if after posterior dislocation of hip. Bone scan photopenic then increased activity with revascularisation/repair/OA. H-shaped vertebra in sickle cell and Gaucher’s disease from involvement of middle superior and inferior endplates. Tx best done early with core decompression (lucency from femoral neck into head) ± vascularised fibular graft.

Specific diseases:

  • Kummell’s disease – AVN of vertebral body with increased density, collapse and gas within the body (vacuum phenomenon).
  • [[Paediatric_Musculoskeletal#Perthes Disease|Legg-Calve-Perthes disease (LCP)]] – AVN of paediatric femoral head.


Orignially thought to be AVN, some now thought to be from mostly traumatic aetiology with subchondral insufficiency fracture (SIF). ?SIF leads to osteonecrosis. Skeletally immature or young adults, M>F (except Freiberg infraction). Includes some normal variants. Bony fragmentation within lucent bed, flattening of articular surface. Overying cartilage usually intact.

  • Kienbock/lunate malacia – True AVN of lunate, associated with negative ulnar variance.
  • Kohler disease – Navicular. Children, painful (cf painless normal variant of fragmented ossification).
  • Freiberg infraction/disease – True AVN with subchondral collapse 2nd-4th metatarsal heads. Compensatory hypertrophy of proximal cortex. Teenage females ?microtrauma from high-heeled shoes.
  • Scheuermann disease – Ring epiphyses of spine.
  • Osgood-Schlatter disease (surfer’s knees) – Tibial tubercle, painful 10-15yo. DDx normal variant fragmented ossification.
  • Sinding-Larsen-Johansson disease – Lower pole patella, painful, 10-15yo.
  • Blount disease – Medial tibial metaphysis.
  • Osteochondritis dessicans (OCD), SONK.
  • Panner’s disase – Capitellum, type of OCD.
  • Sever’s phenomenon/disease – Normal variant fragmented calcaneal apophysis.
  • Van Neck’s phenomenon – Irregular ischiopubic synchondrosis.

Osteochondritis Dissecans (OCD)

Children and teenagers. Type of osteochondral defect ?form chronic stress/injury with SIF then osteonecrosis. Affects subchondral bone, extending to overlying cartilage. Mostly LAME (lateral aspect medial femoral condyle); others include patellar, other femoral condyle surfaces, dome of talus (esp medial), distal capitellum (Panner’s disease), humeral head. Subchondral oedema -> subchondral microfractures coalescing into fracture line paralleling cortex (SIF) -> extension to cortex interrupting blood supply to fragment -> disruption of cartilage (in-situ loose body) -> sloughed off forming displaced loose body/’joint mouse’. Features of instability include high T2 cleft (granulation, oedemous fibrosis or fluid) around most of the fragment, subcortical cyst, bone marrow oedema deep to the fragment, joint contrast extending around fragment, cartilage defect >5mm. In-situ loose body if high T2 surrounds the entire fragment. Enhancement suggests intact blood supply with good potential resolution. Fragment may undergo ostenecrosis with sclerosis. Tx stable lesions NWB; unstable lesions surgery with subchondral pin fixation, or removal and debridement of crater ± osteochondral transplant.

Fragmentation of posterior femoral condyles may be a normal varient, but occasionally progress to OCD.

Hypertrophic Osteoarthropathy (HOA)

Arthralgia of unknown aetiology. XR normal or soft tissue swelling/effusions, symmetric diaphyseal and metaphyseal periosteal reaction (onion skinning, irregularity or waviness with thickness and extent dependent on duration of disease). No erosive or productive changes. DDx thyroid acropachy (surgical resection for hyerparathyroidism, more feathery and spiculated periostitis predominately hands and feet), vascular insufficiency. Suggest CXR for underlying cause.

  • Primary HOA (pachydermoperiostitis) – Ranging from just periostitis to clubbing, skin thickening (esp forehead, dorsum of hands). Familial, M>F, starts in adolescents and usually arrests in young adulthood.
  • Secondary HOA – From bronchogenic carcinoma, other lung tumours (eg pleural fibroma) or chronic suppurative lung disease eg bronchiectasis (hypertrophic pulmonary osteoarthropathy HPOA); cyanotic heart disease, chronic GI disease (biliary cirrhosis, IBD). ?Humoral or neurologic mediator as a cause. Finger clubbing, periostitis usually in extremities. Thoracotomy may result in immediate clinical remission with slower radiographic resolution.