Osteoarthritis: Causes

Pathogenesis (development of disease)

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 apoptosis (programmed 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, sports* or due to obesity. 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
  • Malalignment (varus – valgus)
  • 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 (TNF-α); IFN-γ/interferon-gamma), growth factors and neuropeptides appear during this process. The mediators stimulate proinflammatory (“pro-inflammatory”) cytokines, among others. The pathogenesis of osteoarthritis can be represented as a three-stage process.

  1. Phase (= preliminary stage of osteoarthritis; prearthrosis): here is still a healthy joint, on which, however, already unfavorable influencing factors act, which can favor the development of osteoarthritis as risk factors (see above).
  2. Phase: the respective influencing factors (see above) lead to arthritic changes that are not yet noticed for the affected person.
  3. Phase: here the changes exceed a not exactly determinable measure and by “destructive processes” complaints occur, which are usually indicated joint.

Etiology (causes)

Biographical 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
      • 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.
  • Gender – Women are more likely to suffer from osteoarthritis than men. One suspected cause is the hormonal changes during menopause (menopause).
  • Age – age-related cartilage degeneration due to reduced metabolic activity.
  • Occupations – occupations with long-lasting heavy physical loads (e.g. construction workers, especially floor layers; soccer players).

Behavioral causes

  • Consumption of stimulants
    • Alcohol – ≥ 20 glasses of beer/week lead to a significant increase in coxarthrosis (hip osteoarthritis) and gonarthrosis (knee osteoarthritis); individuals who drank 4 to 6 glasses of wine per week had a lower risk of gonarthrosis
    • Tobacco (smoking) – nicotine abuse promotes loss of articular cartilage in the knee joint (gonarthrosis)
  • 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 (e.g., soccer players).
      • Long-lasting heavy physical stress
  • Overweight (BMI ≥ 25; obesity) – leads to overuse of the joints.

Disease-related causes

  • Congenital/misformity
    • Joint axis displacement – e.g., scoliosis (S-shaped spine), pelvic tilt, knock knees, flat feet.
  • Malalignment (varus – valgus).
    • Coxa valga luxans – flat socket formation.
    • Subluxation (incomplete dislocation) – e.g. hip, knee.
    • Growth disorders in the epiphyseal region (area of the growth plates).
  • Endocrinological disorders/diseases
    • Acromegaly – endocrinological disorder caused by overproduction of growth hormone (somatotropic hormone (STH), somatotropin), with marked enlargement of the phalanges or acras, such as the hands, feet, lower jaw, chin, nose and eyebrow ridges.
    • Hyperparathyroidism (parathyroid hyperfunction).
  • Metabolic disorders/diseases
    • Chondrocalcinosis (synonym: pseudogout); gout-like disease of the joints caused by deposition of calcium pyrophosphate in cartilage and other tissues; leads, among other things, to joint degeneration (often of the knee joint); symptomatology resembles an acute gout attack
    • Gout (arthritis urica/uric acid-related joint inflammation or tophic gout)/hyperuricemia (increase in uric acid levels in the blood).
    • Hemochromatosis (iron storage disease).
    • Ochronosis – deposition of homogentisic acid in the skin, connective tissue and cartilage.
    • Rickets (synonym: English disease) – disease of growing bone with impaired mineralization of bones and disorganization of growth plates in children.
  • Chronic arthropathy – a number of diseases can lead to secondary joint disease. Both inflammatory and non-inflammatory processes can play a role. Examples include joint changes in hyperuricemia (gout) – uric acid-related, diabetes mellitus – glucose-related, hemophilia (bleeding disorder) or leprosy.
  • Inflammatory joint diseases
  • Rheumatic joint diseases
  • Post-traumatic (after joint trauma/joint injury; dislocation – dislocation/dislocation).

Laboratory diagnoses – laboratory parameters that are considered independent risk factors.

Operations