- Jin X, Beguerie JR, Zhang W, Blizzard L, Otahal P, Jones G, Ding C: Circulating C reactive protein in osteoarthritis: a systematic review and meta-analysis. Ann Rheum Dis. 2015 Apr;74(4):703-10. doi: 10.1136/annrheumdis-2013-204494. epub 2013 Dec 20.
Pathogenesis (disease development)
Age-related wear and tear is not the cause of osteoarthritis; rather, acute damage to articular cartilage from trauma or infection is usually at the beginning of joint destruction. Insufficient matrix synthesis and/or increased cell death of chondrocytes (cartilage cells) are discussed as pathogenetic mechanisms.The following pathomechanisms can be observed in osteoarthritis:
- Osteoarthritis due to excessive stress on the joint.
- Osteoarthritis due to inferior bone or cartilage.
Primary osteoarthritis occurs as a result of direct or indirect overloading of the joints.Direct overloading occurs during heavy work or sports* . Indirect overloads include a reduction in cartilage regeneration due to aging or metabolic disorders.Another cause of primary osteoarthritis is joint laxity (joint instability). * Sport, however, is only healthy as long as joints are not damaged in the process or there are no pre-existing conditions. Secondary osteoarthritis can occur as a result of:
- Congenital / malformation
- Malposition
- Endocrinological disorders/diseases
- Metabolic disorders/diseases
- Inflammatory joint diseases
- Chronic inflammatory and non-inflammatory arthropathy (joint disease).
- Rheumatic joint disease
- Post-traumatic (after joint trauma/joint injury; dislocation – dislocation/dislocation).
- Operations
Rhizarthrosis usually occurs spontaneously, that is, there are usually no links to previous trauma (injury) or inflammatory or rheumatic diseases.
- Operations
Osteoarthritis and inflammation (inflammation).
Low-grade inflammation seems to play a greater role in osteoarthritis (English osteoarthritis) than radiological changes in terms of osteoarthritis (signs of degeneration). This was shown by the determination of hs-CRP serum levels (high sensitivity CRP; inflammation parameter), which were slightly but statistically significantly increased compared to the control group.Clinically, about 50% of osteoarthritis patients show signs of synovial inflammation. The signs of synovitis (inflammation of the synovial membrane) are detectable even with minor symptoms and only limited structural changes. A typical immune cell infiltration with monocytes/macrophages and T lymphocytes (CD4 T cells) can be detected. Furthermore, cytokines (tumor necrosis factor-alpha (TNF-α); IFN-γ/interferon-gamma), growth factors and neuropeptides appear during this process. The mediators stimulate proinflammatory (“proinflammatory”) cytokines, among others.
Etiology (causes)
Biographic causes
- Genetic burden from parents, grandparents: e.g., vitamin D receptor (VDR) gene polymorphisms.
- There were significant associations between VDR apal polymorphisms and osteoarthritis in the Asian population, but not in the overall population
- There was also a statistically significant association between FokI polymorphisms and osteoarthritis; however, this result was derived from only two studies
- Age – age-related cartilage degeneration due to decreased metabolic activity.
- Occupations – occupations with long-lasting heavy physical loads (eg construction workers).
Behavioral causes
- Physical activity
- Underloading of the cartilage:
- Lack of physical activity – since cartilage gets its micronutrients from the synovial fluid, it relies on the joint being moved for cartilage growth
- Nutritive damage (eg, long rest in a cast).
- Overload of the cartilage, e.g., by competitive and high-performance sports or long-lasting heavy physical loads.
- Underloading of the cartilage:
Disease-related causes
- Inflammatory joint diseases
- Gout (arthritis urica/uric acid-related joint inflammation or tophic gout)/hyperuricemia (elevation of uric acid levels in the blood)
- Rheumatic joint disease
- Post-traumatic (after joint trauma/joint injury).
Laboratory diagnoses – laboratory parameters that are considered independent risk factors.
- Hyperuricemia (elevation of uric acid levels in the blood).