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British Medical Books Health Issues Computerized Tomography

Os Odontoideum (Degenerative Joint Disease)


  • chronic non-inflammatory disorder of joints
  • characterised by:
    • articular cartilage softening & destruction
    • new bone formation at the joint surfaces & margins (osteophytes)
    • subchondral sclerosis & cysts
    • capsular fibrosis
  • usually dx.of advancing age
  • if in young - underlying pathology
  • more common in some joints (hip, knee & spine) than in others (elbow & ankle)
  • terminal inter-phalangeal OA chiefly affects postmenopausal women (Heberden nodes)
  • different in ethnic groups
    • OA of the hip rare in Africans
    • common in southern European women - high incidence of acetabular dysplasia


  • primary or secondary

Etiological factors

    • obesity
    • genetic & hereditary forms (dysplastic hip, Mseleni hip dx)
    • occupation (IPJ’s in cotton mill workers)
    • endocrine disorders eg. diabetes, acromegaly
    • metabolic disorders eg. Paget’s, gout, CPPD

Increased stress (load per unit area)

  • local mechanical factors
  • 76 % underlying cause for hip OA
    • dysplasia
    • Perthes
    • SCFE
  • >> load
    • deformities affecting the lever system
  • << contact area
    • joint incongruity or instability

Weak cartilage

  • stiff
    • ochronosis
  • soft
    • inflammation (RA, TB etc.)
    • crystal arthropathies

Abnormal support (subchondral bone)

  • osteonecrosis - AVN
  • soft bones
    • dysplasias
    • OI
    • Paget’s


  • cartilage ageing occur
    • splitting & flaking of the surface
    • diminished cellularity
    • reduction of the proteoglycan ground substance & loss of elasticity with decrease in breaking strength
    • proteoglycan matrix depletion - release of proteolytic enzymes - collagen failure - chondrocyte damage - cartilage deformation
  • articular cartilage distributing forces associated with joint loading
  • when loses its integrity ->> forces concentrated in the subchondral bone
    • cyst formation & reactive sclerosis in the zone of maximal loading
  • as the articular surfaces become increasingly mal-apposed & the joint unstable
    • osteophyte formation


Cardinal features

  1. progressive cartilage destruction
  2. subarticular cyst formation
  3. sclerosis of the surrounding bone
  4. osteophyte formation
  5. capsular fibrosis
  • initially confined to one part of the joint - the most heavily loaded part
  • softening, fraying, or fibrillation of cartilage (chondromalacia)
    • joint space narrowing
  • progressive disintegration of cartilage -> underlying bone becomes exposed
    • subchondral sclerosis & cysts
  • joint capsule shows thickening & fibrosis
  • osteophytes arise from the edge of the articular surface as bony outgrowths
  • marked vascularity & venous congestion -> pain

Clinical features

  • usually present after middle age
  • one or two of the large weight-bearing joints (hip or knee)
  • interphalangeal joint (especially in women)
  • any joint that has suffered a previous affliction (CDH, osteonecrosis or intra-articular #)
  • family history common in patients with polyarticular OA


    • usual presenting symptom
    • may be referred to a distant site
    • usually starts insidiously & increases slowly over months or years
    • aggravated by exertion & relieved by rest
    • worst is pain in bed at night
    • causes of pain: capsular fibrosis, muscular fatigue, vascular congestion & intra-osseous hypertension


    • common
    • characteristically it occurs after periods of inactivity - early morning stiffness
    • with time becomes constant & progressive


    • from capsular contracture or joint instability
    • may have preceded and contributed to the onset of OA

Loss of function

    • limp
    • difficulty in climbing stairs
    • restriction of walking distance
    • progressive inability to perform everyday tasks or enjoy recreation
  • typically, the symptoms of OA follow an intermittent course with periods of remission


  • swelling & deformity
  • scars denote previous abnormalities
  • muscle wasting
  • local tenderness
  • fluid, synovial thickening or osteophytes may be felt
  • ROM always restricted
    • hip extension, abD & IR
    • can be crepitus
  • joint instability
    • loss of cartilage and bone
    • asymmetrical capsular contracture
    • muscle weakness

Laboratory findings

  • 1° OA - usually none
  • 2° OA - may see changes (e.g. Paget’s ->> ALP, gout ->> uric acid)
  • synovial fluid - non-inflammatory


Four cardinal signs

    • asymmetric narrowing of the joint space
    • sclerosis of the subchondral bone
    • cysts
    • osteophytes at the margins of the joint
  • X ray changes & correlation to pathology
    • decreased joint space - cartilage erosion
    • subchondral sclerosis - bone eburnation
    • subchondral cysts - synovial fluid intrusion into bone probably as a result of micro#’s
    • osteophytes - revascularization & endochondral ossification of remaining cartilage
    • loose bodies - osteochondral fragmentation
    • deformity & malalignment - destruction of capsule & ligaments
  • may be evidence of previous disorders (congenital defects, old #, RA, chondrocalcinosis)

Bone scan

  • Tc99m-HDP
  • increased activity during the bone phase in the subchondral regions of affected joints
  • vascularity & new bone formation


Monarticular & Pauciarticular OA

  • classic form
  • presents with pain & dysfunction in one or two of the large weight-bearing joints
  • may be an obvious underlying abN - acetabular dysplasia, old Perthes' dx or slipped epiphysis, a previous fracture or damage to ligaments or menisci
  • in the majority - abnormality is more subtle

Polyarticular (generalized) OA

  • most common form
  • usually a middle-aged woman
  • presents with pain, swelling & stiffness of the finger joints, 1st carpo-metacarpal & big toe MP joint, or the knees & lumbar facet joints
    • DIP joint - Heberden’s nodes
    • PIP - Bouchard’s nodes
  • strong association with carpal tunnel syndrome and isolated tenovaginitis
  • X-rays show the characteristic features of OA

OA in unusual sites

  • uncommon in the shoulder, elbow, wrist, MP joints, lesser toes
  • predisposing factors
    • local disorders - intraarticular #, instability, osteochondritis dissecans or AVN
    • crystal arthropathies - OA of shoulder, elbow or patellofemoral joint
    • congenital (e.g. multiple epiphyseal dysplasia)
    • sometimes go undiagnosed until OA presents

Endemic OA

  • affecting entire communities it
  • environmental factor

Kashin-Beck disease - Russia, China

Mseleni joint disease - OA of the hips

    • genetically determined form of multiple epiphyseal dysplasia in both sexes
    • progressive protrusio acetabuli of unknown aetiology in the women

Rapidly destructive OA

  • rapid progression of bone destruction
  • analgesic arthropathy & indomethacin hip
    • drugs suppress prostaglandin synthesis - inhibit healing of microfractures
  • crystal arthropathy

Neuropathic joint disease (CHARCOT’S joint)

  • most destructive arthropathy
  • associated with lack of pain sensibility & position sense
  • lack of N reflex safeguard against abN stress or injury - subchondral bone disintegrates
  • C/O weakness, instability, swelling & progressive deformity
  • X-rays show gross bone erosion and irregular calcified masses
  • underlying neurological conditions include tabes dorsalis, syringomyelia, myelomeningocele and peripheral neuritis (DM)
  • leprosy & congenital indifference to pain are other possibilities

Differential diagnosis

Avascular necrosis

    • x-ray shows preservation of the joint space

Rheumatoid arthritis

    • X-rays show an erosive arthritis with minimal or no osteophytes
    • other joints are affected
    • systemic features

Psoriatic arthritis

    • involve the terminal finger joints
    • an erosive arthritis causing marked destruction & no osteophytes


    • polyarticular gout produces knobbly finger joints
    • bumps d/t tophi
    • x-rays - periarticular bone destruction

Diffuse skeletal hyperostosis (DISH)

    • fairly common disorder of middle-aged people
    • bone proliferation at ligament & tendon insertions around peripheral joints and the intervertebral discs


    • large bony spurs easily mistaken for osteophytes, but bone spurs are symmetrically distributed
    • especially along the pelvic apophyses and throughout the vertebral column
    • sometimes changes confined to spine (ankylosing hyperostosis or Forestier’s dx)

Treatment of OA

  1. symptoms characteristically wax and wane & pain may subside spontaneously for long periods
  2. some forms of OA (e.g. Heberden’s nodes) become less painful with time
  3. recognition (from serial x-rays) of rapidly progressive type of OA may warrant an early move to reconstructive surgery

Early - Non-operative

Pain relief

  • analgesics & NSAIDs
  • local warmth
  • rest periods and modification of activities


  • programme of exercises
  • reduces capsular strain

Load reduction

  • weight loss
  • walking stick
  • avoidance of unnecessary stress (such as jogging or climbing stairs)


  • cell - chondrocyte cultures
  • growth factors

Operative - Intermediate / Late

  • if symptoms & signs increase
  • progressive joint destruction, with increasing pain, instability & deformity

Joint debridement

    • arthroscopic or open
    • remove lose fragments, osteophytes, synovium, irrigation

Alteration of joint loading

  • muscle release
  • realignment osteotomy
    • joint is still stable and mobile
    • x-rays show that a major part of the joint space is preserved
    • pain relief dramatic
        1. vascular decompression of the subchondral bone
        2. redistribution of loading forces towards less damaged parts of the joint
        3. fibrocartilage may grow to cover exposed bone

Penetration of subchondral bone

  • drill-holes
  • fibro-cartilaginous repair

Reconstructive surgery

  • arthrodesis
  • arthroplasty
    • resection - Keller’s, Fowler’s, Girdlestone
    • ST grafts - CMC thumb, elbow
    • cartilage grafts
    • joint replacement

Complications of OA

  • deformity, angulation
  • subluxation, instability
  • stiffness, ankylosis
  • IA loose bodies

common diseases in which 20 OA may occur:

  • trauma - acute & chronic
  • haemochromatosis
  • acromegaly
  • HPT
  • hemophilia
  • neurological diseases eg. diabetes
  • Heberden’s node = bony enlargement at DIP of hands
  • Bouchard’s node = boy enlargement at PIP

OA of CMCJ of the thumb

  • OA of trapezioMC joint is common in females > 50 years
  • pain at the base of the thumb
  • loss of grip strength & ROM

Causes of OA in the wrist:

  • Kienbock’s
  • trauma
  • non-union of the scaphoid
  • gout
  • CPPD
  • carpal instability

The AC joint is the most commonly involved joint at the shoulder
DISH = diffuse idiopathic skeletal hyperostosis:

  • significant osteophyte formation
  • calcification on anterior longitudinal ligament & peripheral disc margins
  • NB - disc height is maintained
  • usually asymptomatic, may be some stiffness of the spine, seldom have pain
  • calcification in the sacrotuberous, iliolumbar & patellar ligaments
  • may be confined to the right side
  • may have calcaneal spurs & marginal osteophytes