1- General risk factors for osteoarthritis:
* Advanced age
* The female
* Hormonal status after menopause
* Overweight
* A dietary deficiency of vitamin D and C
* Family history of first degree
2- The synovial fluid:
a- Normal fluid:
citrine yellow viscous liquid
<300 cells / mm3
30 g / L of protein crystal absence of sterile
b- Mechanical liquid:
citrine yellow viscous liquid
<1000 white blood cells / mm3 with less than 50% of PNN
30 g / L of protein crystal absence of sterile
c- Liquid inflammatory:
+/- Disorder; very fluid
> 1000 or 2000 GB more than 50% of NNP
3- Radiological Semiotics:
* The narrowing of the joint space (sign of destruction of cartilage)
* Osteophytes (bone construction signs) are bony elements appearing at the boundary of the joint
* Bone condensation (bone building sign) appears in the localized pressure areas facing the clamping. It is triangular
* The subchondral geodes (bone destruction marks) appear in the condensation zones
4- Pathophysiology:
– Initial stage: when a persistent hypertension, cartilage responds by overhydration which reflects the high activity of chondrocytes.
They produce excessive proteoglycans trapping water. This excess distends the collagen fibers and soften the cartilage.
– State Stadium: hypercatabolism by releasing enzymes -> matrix degradation.
Local proinflammatory cytokines inhibit the anabolic response of chondrocytes and stimulate the release of enzymes by the synovial.
There is also a production of abnormal proteins (collagen type II not).
Chondrocytes become disorganized (disappearance of columns of chondrocytes) and some to apoptosis.
So there is an imbalance between anabolism and catabolism in activated chondrocyte.
At this stage the subchondral bone reacts to excessive pressure by producing osteophytes.
– Final stage: the successive stages of destruction down deep and lead to exposure of the subchondral bone.
5- Etiologic classification:
* Structural Osteoarthritis: the mechanical forces exerted are normal but the cartilage is of lesser quality (relative hypertension).
It may be idiopathic; metabolic (but never gout); contusion or direct trauma to the cartilage; … hyperparathyroidism.
* Mechanical or secondary Osteoarthritis repeated microtrauma; dysplasia (acetabulum); instability (laxity); articular incongruity (meniscectomy); obesity….
6- Clinqiue:
* The pain is mechanical; it appears to support effort.Absence of nocturnal spontaneous pain.
* Joint stiffness: only appears late and starts very insidious and progressive way.
* The joint effusion: there frequently; scarce.
BIOLOGY:
There is no general inflammatory syndrome
Note: Anti-arthrosis: chondroitin sulfate; diacerein, unsaponifiable extracts of avocado-Sodja.
* Note (out of context)
* Any febrile acute monoarthritis is arthritis until proven otherwise
* Reactive arthritis: Arthritis aseptic occurring in response to a sexually transmitted infection or gastrointestinal infection and the staff of spondyloarthritis.
They are associated with a particular genetic predisposition (HLA B27 in 70% of cases).
Joint involvement is usually in the form of oligoarthritis (80% of cases).
The onset is sudden and joint inflammation is important.
Arthritis are asymmetrical preferentially affecting the knees and ankles.
The achievement of a finger / toe with diffuse inflammation makes appearance suggestive sausage.
The association with signs of axial disease (lumbago, buttock pain) and / or heel pain is suggestive.
The extra-articular involvement is inconsistent or contemporary who preceded arthritis combines 1 month: dysentery (Shigella, Yersinia, Salmonella); urethritis (Chlamydia trachomatis) often bilateral conjunctivitis; balanite (or mouth sores); psoriasiform skin lesions.
The Fiessinger Reiter syndrome (FLR) or Reiter’s disease is a particular clinical form combining conjunctivitis, urethritis, arthritis (ocular urethrovaginal synovial triad)
* Gonococcal arthritis: 2 guide elements, tenosynovitis of the extensor digitorum and papular skin lesions or vesicular-papular.
You must be logged in to post a comment.