Biomechanics of Physiological and Pathological Bone Structures

In 1995 Kuttner and Goldberg defined osteoarthritis as a group of distinct simultaneous diseases, which may have different etiologies but have similar biologic, morphologic, and clinical outcomes. The disease processes does not only affect the articular cartilage, but involve the entire joint, including the subchondral bone, ligaments, capsule, synovial membrane, and periarticular muscles. Ultimately, the articular cartilage degenerates with fibrillation, fissures, ulceration, and full thickness loss of the joint surface (Kuttner & Golderg, 1995). Osteoarthritis (OA) is also characterised by chronic degradation of articular cartilage and hypertrophy of bone tissue in joint region. OA results from both biological and mechanical causes which lead to instability of bone degradation and remodeling processes of entire joint organ, including the chrondocytes, subchondral bone and synovium articular (Grynpas et al., 1991). Precise classification of joint degeneration is difficult. For example, American College of Rheumatology (ACR) classifies osteoarthritis as non inflammatory condition despite the fact, that clinical observation show frequent inflammatory reaction (Pelletier et al., 1999; Wang et al., 2002; Malcolm, 2002) although the latter may actually be a manifestation of a superimposed crystalline arthritis. To evaluate degradation of joint cartilage two methods are the most frequently used: Altman scale (Altman et al., 1986) and Kellegren-Lawrence scale. First method differentiates between primary and secondary effects of degradation without taking into account etiological factors which precise identification allows to prevent development of OA. Kellegen-Lawrence defined a five level scale that is used to evaluate changes in tissue structure based on its images. Unfortunately, if computer tomography images are used then only advanced stages of OA disease can be detected. Origins of OA are not well known but several hypothesis on its etiology were proposed. Hypothesis focus on changes in biochemical composition and physical properties of synovial fluid that debilitates cartilage nutrition, increased friction of joint surface, impaired blood supply as well as increased number of micro–cracks, especially in subchondral bone. When OA affects hip joint then those changes apply to the femoral head and acetabulum. Two, seemingly equivalent hypotheses about the origins and progress of osteoarthritis are presented in the literature (Radin, 1995). According to the first one changes in the articular cartilage cause