Osteoarthritis and joint pain

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Osteoarthritis and joint pain

• R2 ???

2
Osteoarthritris

• m/c articular disorder
• leading cause of persistent musculoskeletal pain
• leationship between Sx. and underlying pathology
• not straightforward

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Classification and pathology

• prior to 1986 no definition existed
• OA degenerative condition involing articular
  cartilage and subchondral bone
• RA disorder of synovial membrane
• current OA is a syndrome with many complex
  etiologies rather than a single disease entity
• joint pain and radiological abnormality
  concordance is poor

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• OA as a pathological aspect
• focal areas of damage to the articular
  cartilage, changes in subchondral and marginal
  bone as well as variable synovitis and capsular
  thickening
• OA as a radiological aspect
• may be normal in some symptomatic individuals
• narrowing of the joint space, osteophyte and
  changes in the subchondral bone
• in lt40, radiographic evidence of OA is rare but
  in gt60, 75

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Osteoarthritis and pain

• 40 pts of severe radiographic change Sx. free
• community-based study inconsistent relationship
  between the magnitude of radiographic change and
  severity of joint pain and accompanying
  disability
• pain, short lived stiffness after inactivity,
  crepitus and swelling
• use-related pain characteristic but may be also
  with rest pain and night pain
• pain aching or throbbing interspersed by
  activity of sharp and stabbing pain

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• risk factors
• inc. age
• female gender
• genetic component
• nutritional deficiency
• joint injury and previous surgery
• obesity, muscle weakness and occupation
• psychological aspect
• strongest predictors of pain severity
• anxiety, depression, hypochondriasis and
  negative emotion

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Mechanisms contributing to pain

• not always caused by local pathology
• referred from proximal structures or pain from
  peri-articular problems
• nerve bundles arising from joints unresponsive
  to strong pressure or either benign or noxious
  movement
• imply need to additional factors such as
  mediators released from synovium or bone

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Local mechanisms

• synovial inflammation role in payhogenesis of
  pain
• joint effusion and popliteal cysts associated
  with inflammation
• synovial thickening and large effusion occur
  more in pt with pain
• generalised uptake of radionuclide correlated
  with self-reported pain
• raised intra-osseus pressure associated with
  OA pain
• bone marrow lesion more prevalent in pt with
  pain

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Neurogenic responses

• changes in central modulation of nociceptive
  input can cause Sx. in OA
• referred pain and tenderness of normal tissue
• inject of local anesthetics result in relief in
  opposite site pain
• associated with muscle hyperalgesia
• lower pain thresholds for pressure stimulation

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Neuromuscular responses

• impaired propioception associated with pain
  than radiological OA

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Therapy

• no effective preventive strategies
• Tx. directed to
• controlling Sx.
• maintaining function
• reducing further joint damage
• core component manage
• lifestyle modification exercise (aerobic and
  strengthening) and weight reduction
• braces and orthtics

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• pharmacological Tx.
• some controversial
• NSAIDS is more preferred but modest supiriority
  over AAP
• weaker opioid codeine with AAP
• topical NSAIDS and intraarticular steroids or
  hyaluronan
• anti-tumor necrosis factor or IL-1 receptor
  antagonist
• doxycycline disease progression can be
  ameliorated
• joint replacement pt with intractable Sx.

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Conclusions

• OA is a heterogeneous joint syndrome involving
  numerous predisposing and biomechanical factors
  that vary from individual to individual
• based on
• mechanical disruption of soft tissue
• intra-articular injection of toxic substances
• genetic modification of structural proteins

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• pain associated OA
• at least maintained by peripheral factors
• central mechanism influencing the individual
  pain experience and associated disability
• coordinated approach and Tx. specific to pt. is
  required