Osteoarthritis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:
Overview
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Pathophysiology
Osteoarthritis (OA) is a well-known degenerative joint disease influencing millions of peopleworldwide. Osteoarthritis count as a complex disease caused by changes in the tissue homeostasis of articular cartilages and subchondral bones. The cell/extra-cellular matrix (ECM) and their interactions play an important role in the pathophysiology of articular cartilage and the occurrence of Osteoarthritis; consequently, the main feature of OA is that after this process in involved joint the articular cartilages of involved joint no longer have a normal acting system and for example because of the the extracellular matrix destruction this articular cartilages cannot act as a shock absorber. Different pathogenic mechanisms have been proposed to be responsible for the occurrence of OA. Heredity, obesity, hypoxia, synovitis–capsulitissubchondral bone overload, joint instability (mechanical integrity disturbances) are the most important underlying causes in this regard. In the current pathogenesis of osteoarthritis (OA) all joint tissues including cartilage, bone, synovium, ligamentous capsular structures, and surrounding muscle are involved. OA characterized by structural changes such as: active bone remodeling, synovial inflammation, and articular cartilage degradation leading to the loss of joint function and angular deformity or malalignment. Also, a variety of bio markers in synovial fluid helped to create more clear insight about the biological response of joints to injury but no biomarker have been declared to be reliable for monitoring the development, progression, and response to therapy of OA. Its been reported that certain factors can increase the risk of the OA development such as: hereditary elements, trauma and mechanical stress, joint injury, age, obesity, physical activity, bone mineral density (BMD), congenital anomalies. and, during the last years signaling pathways mad a lot of attention and its been proven that these pathways play important rolls in inflammation in the remodeling subchondral bone, synovium, enzyme activation, and extracellular matrix degradation in articular cartilage.
Subchondral Bone
Osteoarthritis influencing both articular cartilage and underlying bone structures. One of the most common findings in is the subchondral bone plate thickening. The diseased bone becomes brittle and sclerotic; and the frequent turnovers affecting bone quality. There is still a big question about this fact that does the subchondral bone changes happens simultaneously with the changes in articular cartilage or not. Macroscopic changes of the subchondral bone especially in load-bearing areas such as: increased osteogenetic reactions, increased stiffness, and increased density.
Interest in structural remodeling, vascular biology, and osteoblast cytokine expression of subchondral bone in OA has been stimulated by a large number of studies suggestively associating a role for subchondral bone changes in the pathogenesis of OA. Active bone remodeling is associated with the initiation and progression of OA including sclerosis of the subchondral bone plate, alterations in trabecular structure, osteophytes and bone marrow lesions.2-5 Some studies with a guinea pig OA model suggest that subchondral bone changes precede degradation of articular cartilage.6, 7 Additionally, several cytokines have been found in subchondral bone that play major signaling roles associated with cartilage degradation including IL-1, TNF-α and those of the fibrinolytic system including plasminogen, tissue and urokinase plasminogen activators (tPA, uPA), and plasmin.8
A typical finding in horses that exercise at speed is subchondral sclerosis of bone in joints subjected to high weight-bearing impact and shear forces (e.g., carpus and fetlock).3,5 It has been postulated that articular overload, especially of subchondral bone, produces microtrauma, remodeling, hardening, and displacement of the osteochondral line.5 These changes reduce the elasticity and energy-dissipation capacity of the articular cartilage during locomotion.3 Furthermore, the injured tissue fails to heal because of the combined effects of high-impact exercise protocols, a lack of adequate warm-ups and post-exercise stretching, inadequate development of proprioception, working musculoskeletal tissue while it is fatigued, poor neuromuscular training, and inadequate rest intervals.8 The results of these forces are mechanical lesions that affect the joint tissue and its extracellular matrix (ECM),3 which may account for the common finding of OA in fetlock joints of performance horses or in knee joints of human athletes.5 However, OA also affects non–weight-bearing joints, such as those in the hands, spine, shoulders, and temporomandibular joints in humans and other mammals. Consequently, this theory does not completely explain the origin of these lesions, although either misalignment of articular surfaces or abnormalities of deep ligamentous components in the spinal and temporomandibular joints9 may result in abnormal load distribution.
It is still a matter for debate, however, whether the subchondral bone changes occur at the same time as changes in articular cartilage, and thus are causative, or are the consequence of cartilage degradation. Because bone adapts to changes in mechanical forces (Wolff ’s law), subchondral stiffening could be due to normal bone adaptation [20], because loss of articular cartilage would mean that an increased load is transmitted to bone. On the other hand, several researchers [15,47,48] have suggested that bone sclerosis precedes cartilage degradation and that enhanced bone remodeling by abnormal OA osteoblasts is the initiating event that triggers cartilage damage. Evidence in support of that sequence of events is based on in vitro studies of osteoblasts or of isolated chondrocytes [76]. It is not clear how factors released from osteoblasts can act on chondrocytes in vivo, inasmuch as the mineralized bone matrix constitutes a barrier to diffusion. Microdamage or microfracture could initiate vascular invasion [15,81], but healthy articular cartilage contains antiangiogenic factors [87], is resistant to vascular invasion, and is likely capable of repelling any invasion from the subchondral bone. However, OA cartilage has lost its antiangiogenic factors [39] and its resistance to vascular invasion [30,84]. This suggests that changes in the cartilage itself permit vascular invasion to take place. On balance, although the evidence for an association between OA and changes in osteoblasts and the subchondral matrix is strong, the inference that these are causes of OA is as yet controversial (for further details, see Chapter 2).