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Course of osteoarthritis

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Course of osteoarthritis

  1. 1. andpresentCourse of osteoarthritisCourse of osteoarthritis
  2. 2. How to define osteoarthritis There are several "levels" of osteoarthritis:anatomical, radiological and symptomatic Many people have radiologicallyevident but asymptomaticosteoarthritis Osteoarthritis is not necessarilysynonymous with "pain" Thus, of 100 people aged over 65:2Société Française de rhumatologie website:http://www.rhumatologie.asso.fr/04-Rhumatismes/grandes-maladies/0B-dossier-arthrose/A0_definition.aspINSERM (National medical research institute) web site:http://www.inserm.fr/thematiques/circulation-metabolisme-nutrition/dossiers-d-information/arthrose
  3. 3. Chronic degenerative joint disease Osteoarthritis is characterised by: gradual destruction of the cartilage (chondrolysis) remodelling of the subchondral bone marginal osteophytosis and secondary synovial inflammation3Société Française de rhumatologie website:http://www.rhumatologie.asso.fr/04-Rhumatismes/grandes-maladies/0B-dossier-arthrose/A0_definition.aspSellam J, Berenbaum F. Arthrose. Rev Prat. 2011; 61: 675-686External facet stage 4 chondral lesion. Axialimage from a knee CT arthrography.
  4. 4. 4External facet stage 4 chondral lesion. Axialimage from a knee CT arthrography.
  5. 5. What type of osteoarthritis?A distinction is made between: Symptomatic osteoarthritis which causes pain and functional disabilityand is visible on radiographic images Weight-bearing joint osteoarthritis (hip and knee) Non-weight-bearing joint osteoarthritis(hand and shoulder) Primary osteoarthritis Secondary osteoarthritis arising subsequentto other conditions (injury, malformationor metabolic and inflammatory disorders)5Société Française de rhumatologie website:http://www.rhumatologie.asso.fr/04-Rhumatismes/grandes-maladies/0B-dossier-arthrose/A0_definition.aspSellam J, Berenbaum F. Arthrose. Rev Prat. 2011; 61: 675-686
  6. 6. 6Hip osteoarthritissurrounding the hip.Internal and external femorotibialosteoarthritis. Knee CT-arthrography.Rapidly destructive osteoarthritis of the shoulder, frontalimage gadolinium-enhanced T1 MRI sequenceHand and wristMRI: SE T1-weighted,gadolinium-enhanced coronalimage with fatsuppression.
  7. 7. Oedema and fissuresCartilage lesions start with oedema which divides the collagen fibres Superficial fissures appear Chondrocytes try to compensate for the breakdown of the proteinsmaking up the matrix by producing growth factors The fissures then extend down to the subchondral bone, leaving itexposed, The number of chondrocytes drops and their pro-destructive potentialincreases The subchondral bone becomes osteosclerotic at the pressure pointsresulting in the development of cysts Osteophytes (attempted bone repair), also known as bony spurs,develop in marginal areas which are not under pressure7Société Française de rhumatologie website:http://www.rhumatologie.asso.fr/04-Rhumatismes/grandes-maladies/0B-dossier-arthrose/A0_definition.aspSellam J, Berenbaum F. Arthrose. Rev Prat. 2011; 61: 675-686
  8. 8. The role of the chondrocyte Osteoarthritis is not caused by cartilage wear and tearonly Chondrocytes "wake-up" and start to synthesise: pro-inflammatory cytokines (IL-1, TNF) nitrogen monoxide (NO) pro-inflammatory lipid mediators (PGE2) and proteolytic enzymes (metalloproteases or MPPs andaggrecanases) which cause cartilage matrix breakdown8Société Française de rhumatologie website:http://www.rhumatologie.asso.fr/04-Rhumatismes/grandes-maladies/0B-dossier-arthrose/A0_definition.aspSellam J, Berenbaum F. Arthrose. Rev Prat. 2011; 61: 675-686
  9. 9. Imbalance between destructionand synthesisDuring stress, for example when subjected toexcessive mechanical load, the chondrocytemetabolism changes The cell becomes capable of boosting synthesis ofmatrix components and proteolytic enzymes and reduces release of anti-inflammatory mediatorsor metalloprotease inhibitors produced to halt theinflammatory process and prevent cartilagedestruction (TIMP: tissue inhibitor ofmetalloproteinases, an IL-1 receptor antagonist) This imbalance leads to digestion and destruction ofthe cartilage matrix, which is then not renewed at thesame pace as new components are made9Société Française de rhumatologie website:http://www.rhumatologie.asso.fr/04-Rhumatismes/grandes-maladies/0B-dossier-arthrose/A0_definition.aspSellam J, Berenbaum F. Arthrose. Rev Prat. 2011; 61: 675-686
  10. 10. 10According to Maheu 2012
  11. 11. Fine balance between formationand degradationSynoviocytes in the inflammatory synovial membraneand osteoblasts in the subchondral bone are also capableof secreting mediators, thus contributing to destructionof the cartilage Thus, the balance between synthesis and breakdownof the cartilage matrix is upset in favour of cartilagedegradation Once fragments of the matrix are released into thesynovial fluid, the inflammation continues as a resultof chronic activation of chondrocytes and the synovialmembrane Resulting in increased synthesis of pro-inflammatorymediators11Société Française de rhumatologie website:http://www.rhumatologie.asso.fr/04-Rhumatismes/grandes-maladies/0B-dossier-arthrose/A0_definition.aspSellam J, Berenbaum F. Arthrose. Rev Prat. 2011; 61: 675-686According to Piperno 2012
  12. 12. In sum,12Sellam J, Berenbaum F. Arthrose. Rev Prat. 2011; 61: 675-686Imbalance between synthesis and destruction of the cartilage matrixexplaining extracellular matrix lossD’après Sellam 2011
  13. 13. Pain is a measure of increasing damage During these flares, theosteoarthritis is active andinflammatory phenomena occur This is caused by a synovialmembrane reaction: the synovialmembranes job is to cleanse thejoint of the debris created bycartilage breakdown13Knee osteoarthritis, tibial edema and synovialinflammation. FSE T2 sagittal slices.Société Française de rhumatologie website:http://www.rhumatologie.asso.fr/04-Rhumatismes/grandes-maladies/0B-dossier-arthrose/A0_definition.asp
  14. 14. Inflammatory flares Recent change in pain intensity: sudden increase in intensity over a few days pain at night which wakes the patient up morning stiffness lasting more than 15minutes +/-mechanical pain as soon as anypressure is placed on the joint.14Sellam J, Berenbaum F. Arthrose. Rev Prat. 2011; 61: 675-686 Onset of joint effusion Presence of signs of local inflammation: redness
  15. 15. 15According to Sellam 2011
  16. 16. Does osteoarthritis always progressin flares?The natural history of osteoarthritishas not yet been fully elucidatedIt varies widely depending on the jointaffected and the patientOnce diagnosed, it seems to progressin a non linear fashionTwo other patterns of progression have alsobeen described: rapidly destructive osteoarthritis, whichcauses complete destruction of the cartilagewithin 24 months and slowly progressing osteoarthritis,without obvious flares16Sellam J, Berenbaum F. Arthrose. Rev Prat. 2011; 61: 675-686
  17. 17. Evaluation toolsDifferent tools can be used: Visual analogue scales for pain,functional impairment and, in the caseof hand osteoarthritis, aesthetic impact For leg osteoarthritis, maximumwalking distance with and without painand ability to complete daily tasks Quantification of analgesic and NSAIDconsumption Several indices are used for hip or kneeosteoarthritis:• the Lequesne index• the WOMAC (Western Ontario and McMasterUniversities composite index)17 Sellam J, Berenbaum F. Arthrose. Rev Prat. 2011; 61: 675-686
  18. 18. 18According to Sellam 2012
  19. 19. Three progressive disease profiles Slow progress without any obvious Progress in flares alternating with stable periodsand periods of chrondrolysis: most common Rapid progress: rapidly destructive osteoarthritis(total cartilage destruction in 6 to 24 months)19Sellam J, Berenbaum F. Arthrose. Rev Prat. 2011; 61: 675-686In all cases, an inflammatory flare is believed tobe an indication of accelerated cartilage destructionWhich is why it is so important to treat each painful flare

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