Shoulder Osteoarthritis (Omarthrosis): Causes

Pathogenesis (development of disease)

Age-related wear and tear is not the cause of osteoarthritis; rather, acute damage to the articular cartilage from trauma or infection is usually at the beginning of joint destruction. Insufficient matrix synthesis and/or increased cell death of the chondrocytes (cartilage cells) are discussed as pathogenetic mechanisms. In osteoarthritis, the following pathomechanisms can be observed:

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 the reduction of cartilage regeneration due to aging or metabolic disorders. Since the shoulder joint, unlike the joints of the hip and knees, is not a weight-bearing joint, mechanical processes do not play a role in pathogenesis. * Sport is only healthy, however, as long as joints are not damaged in the process or there are no pre-existing diseases. Secondary osteoarthritis may 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

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; 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
    • z. E.g., through 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
    • Genetic diseases
      • Hemochromatosis (iron storage disease) – genetic disease with autosomal recessive inheritance with increased deposition of iron as a result of increased iron concentration in the blood with tissue damage.
  • 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).
    • Overloading of the cartilage:
      • Competitive and high-performance sports
      • Long-lasting heavy physical stress

Causes due to disease

  • Chondromatosis – occurrence of multiple benign tumors in bone (rare).
  • Inflammatory joint disease (rheumatoid arthritis).
  • Humeral head necrosis – change caused by circulatory disturbance of the humeral head.
  • Metabolic disorders/diseases
  • Post infectionem (after healed infections) (rare).
  • Rheumatic joint disease
  • Metabolic disorders such as hyperuricemia (elevation of uric acid levels in the blood).
  • Post-traumatic (after joint trauma / joint injury; dislocation – dislocation / dislocation).
    • Fracture of the humeral head (fracture of the upper end of the humerus).
    • Recurrent (recurrent) dislocation of the shoulder.
    • Rotator cuff damage/altered biomechanics in rotator cuff defects (common).

Laboratory diagnoses – laboratory parameters considered independent risk factors.

Operations

  • Shoulder joint surgery