[Features of the progression and treatment of osteoarthritis]

Authors
Category Primary study
JournalРегулярные выпуски «РМЖ»
Year 2005
The concept of osteoarthritis (OA) as a distinct disease of the joints was made after the publication of Cecil RL and Archer B.H. in 1926. According to the modern definition of the American College of Rheumatology (ACR), OA is a "heterogeneous group of diseases of the joints of different etiology, but with similar biological, morphological and clinical features and outcome, leading to loss of cartilage and concomitant defeat other components of the joint - subchondral bone, synovium, ligaments, periarticular muscle capsule and "[23]. Currently, OA is the most common joint disease. Clinical manifestations observed in more than 20% of the world population, and radiographic signs of the disease are detected much more frequently. The incidence of OA increases with age - people over age 60 are diagnosed in 97%. It predicts that by 2020 the incidence of OA in a population may reach 57%. Particularly alarming data on the growth trends of morbidity by age group younger than 45 years [25]. For many years, OA was considered as an isolated disease of the joints associated with the degeneration of the cartilage as a result of the natural aging of the human body. It is now believed that the basis of the progression of OA is the set of complex interactions with each other causes and mechanisms are only partially related to age-related changes. In recent years, the evidence of the impact on the development of OA genetic predisposition, biomechanical and metabolic changes, local inflammation, etc. [5.18]. According Holdebaum (1999), mutations on chromosome 12 in the molecules of the gene coding for the type II procollagen (COL2A1), associated with a reduction in the strength of the cartilage and are associated with the early development of OA. Progressive cartilage degradation («wear and tear», ie abrasion and cracking) promote occupational hazard related to mechanical factors. Epidemiological studies [Felson D. et al., 1995; Kojola. et al., 1994] have shown that work with bent limbs, lifting and moving heavy loads, walking long distances increases the risk of OA. Given the presence of mechanical risk factors doctors, we examined 400 surgeons and physicians under the age of 50 years. According to a study [3] OA health care workers diagnosed much more frequently than in the population - 36.1% and 13.9%, respectively. The important role of inflammatory component in the progression of OA says even the terminology - abroad, the disease is referred to as «osteoarthritis» ie Osteoarthritis - in contrast to the accepted in Russia the term "osteoarthritis". Local inflammation or development of secondary synovitis often determines the severity of pain in patients with OA and largely determines the quality of their lives. But inflammation in OA has not only clinical but also pathogenetic significance. The expression of a wide range of "pro-inflammatory" contributes to the progression of the disease mediators. [20] The most studied metabolic disorder, significantly increases the risk of OA, is obesity. According to a study in twins (middle-aged women), weight gain of 1 kg is accompanied by an increased risk of gonarthrosis by 9-13% [13]. Less studied is the impact on the progression of OA combination of metabolic disorders, which are allocated to a single syndrome and described under different names - metabolic syndrome, syndrome X, "deadly quartet", etc. The main components of this syndrome is insulin resistance and hyperinsulinemia, glucose intolerance, abdominal, visceral obesity, dyslipidemia, hypertension, hyperuricemia, impaired hemostasis, microalbuminuria, hyperandrogenism. From the perspective of the life prognosis is important that the combination of the above violations greatly accelerates the progression of atherosclerosis, ie, increases cardiovascular risk in this group of patients. All of these factors (and more often - a combination thereof) cause cartilage damage, and thus contribute to the progression of OA (Figure 1).
Epistemonikos ID: caf3c8c5f9a71ef508d55a1a83657fa6bcabde84
First added on: Jul 28, 2015