الفهرس 
Articular cartilage Histology & BiologyOnly 14 pages are availabe for public view
 |  | from | 114 |  |  |
| | | from | 114 | | |
Abstract
Articular cartilage injuries persist indefinitely and can result in poor functional outcome over time. Unfortunately, these injuries are commonly encountered by the practicing orthopedic surgeon. Unfortunately, articular cartilage has a poor intrinsic capacity for healing after injury. Articular cartilage regeneration is poor as the result of its avascular nature and as a result of the extracellular matrix structure of collagen and proteoglycan. This lack of blood flow limits the intrinsic healing process by inhibiting transport of inflammatory mediators to the defect. In addition, the extracellular matrix does not allow cellular migration to the sites of cartilage injury. As a result, even though chondrocytes do respond initially to tissue injury, they are not capable of repopulating the defect; ultimately, these cells cease their attempts at healing the area of injured cartilage. These lesions can become symptomatic and in the long term lead to continued cartilage erosion and osteoarthritis (Williams RJ, 2006).
Articular cartilage can be insulted in various pathological joint conditions such as trauma, inflammation, infection, and degeneration. The type of cartilage injury including its depth and size, and whether it is acute or chronic, distinctly affects the healing response. The prognosis for eventual repair greatly diminishes when there is visible mechanical disruption of the cartilage. The lack of an intrinsic blood supply and the very high proportion of matrix to cellular components are responsible for the generally dismal results. Given the lack of an undifferentiated cell pool within the cartilage substance and the low mitotic activity of chondrocytes in the physiological state, the healing of even a small cartilage lesion places a massive burden on a cell that is sparsely distributed and ill suited for such feats (Jun-Kyo Suh et al, 1995).
The approach to cartilage lesions should be tailored to every individual. Factors contributing to decision making are both patient-specific and lesion-specific: Patient-specific factors include age (physiological rather than chronologic age), body mass index, activity levels/functional demands, systemic inflammatory and immunosuppressive disorders, the intrinsic healing capacity, and ability to comply with rehabilitation. Lesion-specific factors include defect etiology, size, site, containment, and condition of the surrounding cartilage (Haleem & Chu, 2010).
There is no validated treatment algorithm available for the treatment of cartilage lesions. Cartilage repair is a rapidly emerging field that is in constant flux. Such change makes the development of a
treatment standard even more difficult. Currently, there are a number of surgical options for the treatment of articular cartilage lesions. Although some confusion exists as to which procedures work best, there does exist an extensive body of evidence that procedures such as microfracture arthroplasty, mosaicplasty, autologous chondrocyte implantation (ACI), and osteochondral allograft transplantation are effective in restoring joint function (Williams RJ, 2006).
The treatment of isolated articular cartilage lesions remains a difficult clinical.