Abstract
Although osteoarthritis (OA) is the most common musculoskeletal condition that causes significant health and social problems worldwide, its exact etiology is still unclear. With an aging and increasingly obese population, OA is becoming even more prevalent than in previous decades. Up to 35% of the world’s population over 60 years of age suffers from symptomatic (painful, disabling) OA. The disease poses a tremendous economic burden on the health-care system and society for diagnosis, treatment, sick leave, rehabilitation, and early retirement. Most patients also experience sleep disturbances, reduced capability for exercising, lifting, and walking and are less capable of working, and maintaining an independent lifestyle. For patients, the major problem is disability, resulting from joint tissue destruction and pain. So far, there is no therapy available that effectively arrests structural deterioration of cartilage and bone or is able to successfully reverse any of the existing structural defects. Here, we elucidate novel concepts and hypotheses regarding disease progression and pathology, which are relevant for understanding underlying the molecular mechanisms as a prerequisite for future therapeutic approaches. Emphasis is placed on topographical modeling of the disease, the role of proteases and cytokines in OA, and the impact of the peripheral nervous system and its neuropeptides.
Highlights
More than 10% of the world population show clinical symptoms of osteoarthritis (OA), affecting most individuals above the age of 65
Anymore, osteoclast activity extends into the calcified cartilage, vascular ingrowth into the articular cartilage occurs and osteoblasts infiltrate, which deposit novel bone that results in end-stage OA sclerosis [28]
This study indicates that AF patients suffer from hyperinnervation with sensory nerve fibers relative to sympathetic nerve fibers in the anterior compartments of the knee
Summary
More than 10% of the world population show clinical symptoms of osteoarthritis (OA), affecting most individuals above the age of 65. Specific topographical patterns of early articular cartilage and subchondral bone changes are observed after defined OA induction in large animal models resembling phenotypes, as seen in patients [8] These patterns arise locally and progress globally, precisely indicating disease progression, as they progressively disturb the strong tissue connections existing within a normal osteochondral unit. These processes are regulated by a complex network of proteolytic enzymes, chemokines, cytokines and neuropeptides Joint tissues such as the synovium, articular cartilage, meniscus and subchondral bone, including their cellular components, are targets for neuropeptides. It is evident that sensory neurotransmitters have crucial trophic effects, which are critical for joint tissue function and bone homeostasis They modulate articular cartilage, subchondral bone and synovial tissue properties in physiological and pathophysiological conditions in addition to their classical neurological features. The final part elaborates on the contribution and role of sensory neuropeptides in joint tissue pathology and their involvement in modulating inflammatory processes in the joint during OA pathogenesis
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