An essay on the biology of osteoarthritis

Bollet, Alfred Jay

doi:10.1002/art.1780120212

Cited by 73 publications

(23 citation statements)

References 27 publications

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“…By age 75, 85% of the population has radiographic or clinical evidence of degenerative joint disease (Lawrence, 1987;Moskowitz, 1988). The general consensus is that degenerative changes in all components of the temporomandibular joint become more common in both males and females as people age (Blackwood, 1963;Moffett et a!., 1964;Bollet, 1969;Oberg et al, 1971;Carlsson, 1974;Kopp, 1978;BudtzJ0rgensen et al, 1985;.…”

Section: In the Temporomandibular Jointmentioning

confidence: 99%

“…2 and 7). Age-related changes in the temporomandibular joint include: (i) decreased water content (Miles and Eichelberger, 1964;Bollet and Nance, 1966;Mankin and Thrasher, 1975;Grushko et al, 1989;Peyron and Altman, 1992), (ii) decreased cellular proliferation (Hammerman, 1993), (iii) accumulation of senescing cells (Dreesen and Halata, 1990;Hammerman, 1993), (iv) altered, decreased, or lost response to growth factors (Hammerman, 1993), (v) accumulation of altered proteins (Brown and Jones, 1990;Chevalier et al, 1992;Hammerman, 1993), and (vi) decreased catabolic activity (Bollet, 1969). There are also age-related changes that appear to be specific to cartilage, including: (i) decreased cellular density in the prechondroblastic region (Livne et al, 1985), (ii) accumulation of degenerating chondrocytes (Dreesen and Halata, 1990), (iii) reduction in the number and size of proteoglycans (Vasan, 1980;Lash and Vasan, 1983, and references therein), (iv) reduction in the molecular weight of the proteoglycan core protein (Hamerman, 1993), and (v) changes in the size and composition of the glycosaminoglycans (Hjertquist and Lemperg, 1972;Elliott and Gardner, 1979;Roughley and White, 1980;Lash and Vasan, 1983;Mankin, 1984;Hamerman, 1989;Ratcliffe et al, 1993).…”

Section: (3) Induction Of Cellular Stress Responsesmentioning

confidence: 99%

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Pathogenesis of Degenerative Joint Disease in the Human Temporomandibular Joint

Haskin

Milam²,

Cameron

1995

Critical Reviews in Oral Biology & Medicine

136

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ABSTRACT:The wide range of disease prevalences reported in epidemiological studies of temporomandibular degenerative joint disease reflects the fact that diagnoses are frequently guided by the presence or absence of non-specific signs and symptoms. Treatment is aimed at alleviating the disease symptoms rather than being guided by an understanding of the underlying disease processes. Much of our current understanding of disease processes in the temporomandibular joint is based on the study of other articular joints. Although it is likely that the molecular basis of pathogenesis is similar to that of other joints, additional study of the temporomandibular joint is required due to its unique structure and function. This review summarizes the unique structural and molecular features of the temporomandibular joint and the epidemiology of degenerative temporomandibular joint disease. As is discussed in this review, recent research has provided a better understanding of the molecular basis of degenerative joint disease processes, including insights into: the regulation of cytokine expression and activation, arachidonic acid metabolism, neural contributions to inflammation, mechanisms of extracellular matrix degradation, modulation of cell adhesion in inflammatory states, and the roles of free radicals and heat shock proteins in degenerative joint disease. Finally, the multiple cellular and molecular mechanisms involved in disease initiation and progression, along with factors that may modify the adaptive capacity of the joint, are presented as the basis for the rational design of new and more effective therapy.

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Section: In the Temporomandibular Jointmentioning

confidence: 99%

Section: (3) Induction Of Cellular Stress Responsesmentioning

confidence: 99%

Pathogenesis of Degenerative Joint Disease in the Human Temporomandibular Joint

Haskin

Milam²,

Cameron

1995

Critical Reviews in Oral Biology & Medicine

136

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“…Histochemical and biochemical studies of cartilage from osteoarthritic human joints have shown a significant decrease in the GAG content (12)(13)(14)(15)(16)(17), and that the decrease in approximately proportional to the severity of the disease. Since it has also been shown that osteoarthritic cartilage has an increased rate of protein and polysaccharide syntheses (12,17,18), it has been postulated that the observed activity is a "feedback" response related to an increased selective enzymatic degradation of the protein polysaccharides of the matrix (14,15,17,19).…”

Section: Introductionmentioning

confidence: 99%

“…Since it has also been shown that osteoarthritic cartilage has an increased rate of protein and polysaccharide syntheses (12,17,18), it has been postulated that the observed activity is a "feedback" response related to an increased selective enzymatic degradation of the protein polysaccharides of the matrix (14,15,17,19).…”

Section: Introductionmentioning

confidence: 99%

The Glycosaminoglycans of Normal and Arthritic Cartilage

Mankin¹,

Lippiello²

1971

J. Clin. Invest.

190

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A B S T R A C T The cartilages from the hip joints of 13 normal and 15 osteoarthritic humans were analyzed for glycosaminoglycan content and distribution. The GAGs were separated by elution with CPC on a short cellulose column by the technique of Svejcar and Robertson after digestion of the tissue with pronase and papain.The eluates were identified by a variety of methods including determination of molar ratios, N-acetyl-hexosamine determinations after hyaluronidase treatment and thin-layer chromatography of unhydrolyzed and hydrolyzed GAGs.From the data obtained, it was demonstrated that cartilage from arthritic patients showed a significant increase in the concentration of chondroitin 4-sulfate and a significant decrease in keratan sulfate, with only slight changes in the total amount of GAG present. Calculations of the molar ratios showed variation in the sulfation -with chondroitin 4-sulfate appearing in the "supersulfated" state in the arthritic cartilage.The data lead to speculation regarding the process of osteoarthritis, and it is concluded that the changes seen are more likely to represent an altered pattern of synthesis rather than selective degradation. Since the changes suggest a younger cartilage, a theory is advanced that the chondrocyte responds to the chronic stress of osteoarthritis by modulation to a chondroblastic phase.

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“…It is not known what is the primary cause leading to OA, certainly, mechanical and constitutional factors play a role. Some authors believe that the primary lesion occurs in cartilage (Bollet 1969, Lee et al 1974, the subchondral bone (Radin 1973(Radin , 1976, or synovium (Glynn 1977). However, any of these could be the primary event in different pathophysiological pathways to OA.…”

mentioning

confidence: 99%