Hip Osteoarthritis (Coxarthrosis): Causes

Pathogenesis (disease development)

Age-related wear and tear is not the cause of osteoarthritis; rather, acute damage to the articular cartilage from trauma or infection (rare) 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:

The causes of primary coxarthrosis are unknown. It is assumed that the articular cartilage is congenitally inferior. Primary coxarthrosis is often associated with osteoarthritis of other joints, including the lumbar spine. Secondary coxarthrosis develops much earlier than the primary form. There are many causes (see below). The occurrence of bilateral (both sides) coxarthrosis is favored by:

  • Increasing age
  • Diabetes mellitus
  • Joint trauma/joint injury on the opposite side
  • Pre-disease of the joint on the opposite side

Risk factors for unilateral (one-sided) coxarthrosis include:

  • Joint trauma/joint injury
  • Pre-existing joint disease

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 (“proinflammatory”), among other things

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 (e.g. construction workers); esp. lifting and carrying heavy loads for long periods of time (2-2.5 times the risk)

Behavioral causes

  • Consumption of stimulants
    • Alcohol – ≥ 20 glasses of beer/week lead to a significant increase in coxarthrosis and gonarthrosis (knee osteoarthritis); individuals who drank 4 to 6 glasses of wine per week had a lower risk of 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
      • Long-term heavy physical stress, e.g., at work (construction workers, especially floor layers); esp. lifting and carrying heavy loads for long periods of time (2-2.5 times the risk)
  • Overweight (BMI ≥ 25; obesity) – leads to overuse of the joints.

* Sport, however, is only healthy as long as joints are not damaged in the process or have no pre-existing conditions.

Disease-related causes

  • Chronic arthropathy – a number of diseases can lead to secondary joint disease. Both inflammatory and noninflammatory processes may play a role.Examples are joint changes in hyperuricemia (gout) – uric acid-related, diabetes mellitus – glucose-related, hemophilia (hemophilia) or leprosy.
  • Circulatory disorder of the femoral head.
  • Inflammatory joint disease
  • Malalignment (varus – valgus)
    • Coxa plana (hip joint deformity due to flattening of the femoral head (head of the femur)).
    • Coxa valga luxans – flat acetabular formation.
    • Coxa vara (“outwardly bent” hip)
    • Subluxation – incomplete dislocation.
  • Congenital hip dysplasia – congenital maldevelopment of the hip joint.
  • Perthes disease – idiopathic (without apparent cause) infantile necrosis of the femoral head.
  • Post-traumatic events – after joint trauma/joint injury; dislocation (dislocation/dislocation).
  • Rheumatic joint diseases
  • Metabolic disorders such as diabetes mellitus, hyperuricemia (increase in uric acid levels in the blood)/gout.
  • Subluxation – incomplete dislocation of the hip.

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

Further

  • Pelvic obliquity (= leg length difference < 2 cm)?