Effective treatment of osteoarthritic pain, tackling the challenge with pets

Abstract

Pain in joints is a major clinical problem. Among diseases causngchronic jointpain, osteoarthritis (OA) is amore frequent causeof ain than inflammatory joint diseases, such as rheumatoid arthritis 1].While OA is rarely observed in young people (prevalence <0.1% n age group 25–34 years), its prevalence is about 30% in age group 5–74 years and women are more likely to have OA than men [2]. n addition to age, amongmain risk factors of OA are obesity, injury nd congenital anomalies. Obesity increases mechanical stress on he weight-bearing joints, which may explain association of obeitywithOA, althoughacontributionof atypicalhormoneorgrowth actor concentrations that affect the cartilage or bone has not yet een excluded. It has also been speculated that nutrients might lay a role in OA, e.g. by influencing bone mineralization and cell ifferentiation in joints [2]. OA affects joint cartilage and subchondral bone. OA typically eads to loss of articular cartilage, new bone formation in the subhondral region, and formation of new cartilage and bone at the oint margins [2]. Characteristic symptoms of OA are pain, stiffess, functional limitations and reduced quality of life. OA usually nvolves one or a few joints, most frequently knees or hips, and he pain is typically worsened by exercise and relieved by rest. In hysical examination, the OA patient may have deformations and igns of local inflammation, such as joint swelling,whichmay cause ifficulties in differentiating OA from other inflammatory forms of rthritis [2].While OA is associatedwith X-ray abnormalities in the oint, the radiological findings only poorly predict whether the OA atient has pain. However, the correlation of OA pain with strucural abnormalities has been better when using high-resolution agnetic resonance imaging than traditional X-rays [2]. Genetic factors, mechanical stress and age are considered to be mong key factors influencing development of OA [3,4]. At cellular nd molecular levels, multiple mechanisms may contribute to the athogenesis of OA as indicated by the finding that initial stages f OA involve increased cell proliferation and synthesis of matrix roteins, proteinases, growth factors, cytokines and various other nflammatory mediators [3]. Many of the compounds generated n OA are known to sensitize nociceptive nerve fibers innervatng the joint [5]. It is still unclear which cellular and molecular