What are the causes and pathology of osteoarthrosis?

  Osteoarthritis (OA): In 1986, The American College of Rheumatology (ACR) defined osteoarthritis as a heterogeneous group of diseases in which joint symptoms and signs are associated with impaired articular cartilage integrity, subchondral bone changes (including microfractures and cystic changes), and bone redundancy formation at the joint edges. Osteoarthrosis is a heterogeneous group of diseases.
  Osteoarthrosis can be classified as primary or secondary. Secondary factors: metabolic, anatomical abnormalities, traumatic, inflammatory, etc.
  Etiology of osteoarthrosis
  -Age
  It was found that the incidence of osteoarthrosis, whether in the knee, hip or hand joints, increases with age. For every 5 years of age, the incidence of knee osteoarthrosis increases by 20%, and the risk of hip OA in the 70s is 2.38 times higher than in the 50s.
  -Weight
  1.Weight and knee OA are closely related
  2, weight and hip OA relationship is small
  3.The relationship between body weight and OA of hand joint group is uncertain
  -Gender
  1.Knee OA is more common in women than in men
  2.The difference between women and men in hip OA is not significant
  3.The risk of OA in the hand joint group is 2.6 times higher in women than in men
  -Occupational activity
  1.Heavy physical labor
  2.Squatting or kneeling
  3, special occupations (such as constant use of computers, etc.) susceptible to OA of the hand joint
  -Non-occupational sports activities
  1.Soccer has a high incidence of tibiofemoral arthritis, while weightlifting has a high incidence of patellofemoral arthritis
  2. Recreational sports do not increase the incidence of knee osteoarthritis
  3. There is no significant correlation between high-intensity nonprofessional sports and hip OA
   -Hormones
  Estrogen can act directly on cartilage cells or protect cartilage by acting on bone or other tissues
  -Osteoporosis
  1, Bone density is higher in patients with knee or hip OA than in those without arthritis.
  2, Bone density under articular cartilage can affect stress under articular cartilage loading
  -Genetic factors
  Hand OA and knee OA have specific genetic correlation
  -Congenital deformities
  Congenital and developmental malformations such as acetabular dysplasia, internal and external knee deformities
  -Injury
  1, Osteoarthritis may be the result of joint injury
  2. Knee/hip OA, especially unilateral OA, is closely related to injury
  -Meniscectomy
   Meniscectomy increases the risk of knee OA
  -Other
  1, smoking: the correlation with the occurrence of OA is unclear
  2, race: the incidence of knee OA is higher in black American women than in whites
  3, grip strength and hand joint OA related
  The pathological characteristics of osteoarthrosis
  -The pathology is characterized by degenerative destruction of articular cartilage, subchondral bone sclerosis or cystic changes, osteophytes at the joint edges, synovial hyperplasia, contracture of the joint capsule, ligamentous laxity or contracture, and muscle atrophy and weakness.
  -In general, most knee osteoarthropathies have a flexion inversion deformity or valgus deformity
  X-rays show severe medial and lateral articular cartilage destruction, narrowing of the medial or lateral joint space, osteophytes at the knee margins, and subchondral bone sclerosis
  -Knee arthroscopy shows cartilage destruction, synovial hyperplasia, and intra-articular free bodies
  -The extracellular mechanism of the articular cartilage is fissured, the hyaline cartilage is transformed into fibrocartilage, the number of chondrocytes in the softened area of the articular cartilage increases, but at the same time apoptosis occurs, the subchondral bone trabeculae are necrotic and collapsed, a small amount of granulation tissue grows in at the edges, a large amount of fibrotic granulation tissue grows in and replaces the necrotic bone trabeculae, the subchondral bone trabeculae are structurally disorganized and the normal structure is lost. The subchondral bone trabecular structure is disturbed, the normal structure is lost, subchondral pseudocysts appear, at the same time there is new bone formation, bone trabecular proliferation and hardening, appearing bone superfluous or joint rat
  Peripheral soft tissues: corresponding changes in the soft tissues around the joint.