CONVENTIONAL MEDICAL SCIENCE

Conventional medical science

Conventional medical science

Introduction

Osteoarthritis is the most common form of arthritis. Despite the suffix “-itis,” which implies an inflammatory process, the painful joints characteristic of osteoarthritis are due primarily to gradual loss of cartilage rather than inflammation. Cartilage is a form of connective tissue that lines joints and protects the ends of bones from rubbing against one another. It can break down because of physical injury, mechanical stress, or some underlying metabolic abnormality. As a result, bones begin to grate against one another, producing pain and further degeneration. Over time the bones may thicken and additional bone may grow along the sides, producing lumps (bone spurs or osteophytes). Fluid-filled cysts may also develop, and the surrounding area may become inflamed. Osteoarthritis (also called degenerative joint disease or wear-and-tear arthritis) tends to occur in joints most exposed to weight-bearing and stress, especially the spine, knees, hips, thumb, and big toe (Altman, 1973, p. 79).

In this paper, the author will take reference from the book “The complementary therapist's guide to conventional medicine” by Claire Stephenson, along with three other sources in order to examine different aspects of conventional medical science and also compare the Conventional medicine and Alternative medicine.

Discussion & Analysis

Pathophsiology of oteoarthritis

Two principal mechanisms are thought to initiate osteoarthritis (Ryu, 1984, pp. 27-49):

In most patients, the initiating mechanism is damage to normal articular cartilage by physical forces, which can be either single events of macrotrauma or repeated microtrauma. Chondrocytes react to this injury by releasing degradative enzymes and elaborating inadequate repair responses.

Less commonly, fundamentally defective cartilage initially fails under normal joint loading, thereby leading to osteoarthritis. Examples include a type II collagen gene defect or ochronotic cartilage that fails because of deleterious pigment deposition.

The initiation of the osteoarthritic process therefore appears to involve abnormalities in biomechanical forces and/or cartilage. Once begun, the pathway leading to osteoarthritis involves numerous other factors. These include mechanotransduction, the interplay between proteases, protease inhibitors and cytokines on cartilage degradation and mechanisms of cartilage repair, and the contributions from multiple risk factors (such as obesity, aging, mineral deposition, systemic hormones, and abnormalities in neurogenic control) (Hulth, 1972, p 97).

Abnormalities associated with osteoarthritis are not restricted to the articular cartilage. Thickening of the subchondral bone (sclerosis) is a classic radiographic feature, and magnetic resonance imaging has revealed abnormalities in the juxtaarticular bone marrow that correlate with the presence of a relatively increased bone mineral density (Stephenson, 2011, pp. 56-68).

Genetic Predisposition

A variety of genetic studies, ranging from OA prevalence in twins, other siblings, and whole genome scanning techniques suggest that there is a genetic contribution to the risk of developing OA. This genetic aspect of the pathogenesis of OA is discussed in detail elsewhere (Jasin, 1989, p. 86).

Exercise and Mechanical Loading

The interaction between exercise and osteoarthritis of the weight-bearing joints is complex. In vitro, in vivo, and clinical data suggest that, in various forms and degrees, exercise may prevent, cause, accelerate, or treat osteoarthritis.

In general, studies in (human) runners have failed to demonstrate an increased risk for ...