Identification and concentration of the glycosaminoglycans of human articular cartilage in relation to age and osteoarthritis

Hjertquist, Sven‐Olof; Lemperg, Rudolf

doi:10.1007/bf02012552

Cited by 66 publications

(23 citation statements)

References 37 publications

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“…a decrease in the keratan/chondroitin sulphate ratio. On the other hand, a number of authors (Bollet and Nance, 1966;Hjertquist and Lemperg, 1972) have reported the opposite, namely that in fibrillated cartilage there is actually a greater reduction in the chondroitin than keratan sulphate. The reasons for these divergences are not clear at the moment.…”

Section: Chemical Composition Of Femoral Head Cartilage As a Functionmentioning

confidence: 97%

Chemical composition and swelling of normal and osteoarthrotic femoral head cartilage. I. Chemical composition.

Venn¹,

Maroudas²

1977

Annals of the Rheumatic Diseases

479

269

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SUMMARY Radiochemical and biochemical methods were used to characterize post-mortem and osteoarthrotic femoral head cartilage. Fixed charge density measurements were correlated with glycosaminoglycan content as estimated by uronic acid and hexosamine analyses. In post-mortem cartilage water content decreased from a maximum at the surface to a minimum in the deep zones. In the osteoarthrotic specimens water content was greatest in the middle zones. Glycosaminoglycan content increased with depth and in the osteoarthrotic specimens was reduced throughout the depth of the cartilage. With increasing degeneration there was an increase in water content and decrease in glycosaminoglycan content. The difference in the water content profile in osteoarthrotic cartilage was explained in terms of damage to the collagen network. In osteoarthrosis the latter is no longer capable of restraining the swelling pressure produced by the glycosaminoglycans and swelling is greatest in the midzones, where glycosaminoglycan content is highest.Topographical variations in the total glycosaminoglycan content of human cartilage has been studied using the fixed charge density (FCD) method in post-mortem specimens of the hip (Maroudas et al., 1973) and knee (Ficat and Maroudas, 1975). FCD measurements have been correlated with biochemical analyses for cartilage of the human femoral condyle (Maroudas et al., 1969). Chondroitin sulphate showed small variations with depth but keratan sulphate content increased with depth from the surface. Chemical analyses have also been correlated with the distribution of histochemical staining (Stockwell and Scott, 1967). A similar distribution pattern has been described for bovine knee cartilage when the glycosaminoglycans were separated as their macromolecules (Lemperg et al., 1974).The aims of the present study were first to confirm that the FCD as measured by the tracer cation method (Maroudas and Thomas, 1970;Maroudas et al., 1973) agreed over a wide range of concentrations with the values calculated from chemical determinations of uronic acid and hexosamine, and second, to compare topographical variations in the

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Section: Chemical Composition Of Femoral Head Cartilage As a Functionmentioning

confidence: 97%

Chemical composition and swelling of normal and osteoarthrotic femoral head cartilage. I. Chemical composition.

Venn¹,

Maroudas²

1977

Annals of the Rheumatic Diseases

479

269

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“…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). Thus, although the incidence of degenerative joint disease is strongly associated with increased age, the processes involved in the progression of degenerative joint disease are different from, and possibly independent of, aging.…”

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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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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“…Non-weight-bearing areas 4.33 + 1-56 5-61 ± 3-23 7.19 ± 1-5 11-46 ± 1-6 38-5 ± 24-7 170 ± 25 Inferior aspect n = 3 n = 3 n = 3 n = 3 n = 3 n = 3 24 Mitrovic, Gruson, Demignon, Mercier, Aprile, De Seze 1 and 2 were practically all active but to a variable degree. In the zone 3 the proportion of active cells was higher than in normal cartilage, though about 25% of the cells remained inactive (Table 6 and Fig.…”

Section: In Osteoarthrotic Cartilage the Cells From Zonesmentioning

confidence: 99%

Metabolism of human femoral head cartilage in osteoarthrosis and subcapital fracture.

Mitrović¹,

Gruson²,

Demignon³

et al. 1981

Annals of the Rheumatic Diseases

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SUMMARYThe cell density and incorporation of 35S04 and 3H-glycine into human articular cartilage from 8 osteoarthrotic and 7 normal (subcapital fracture) femoral heads were studied. It was found that osteoarthrotic cartilage incorporates on a per cell basis about twice as much 35S04 and 2-5 times as much 3H-glycine as normal cartilage. There was no relationship between the intensity of incorporation and either the location of the cartilage (weight-bearing versus non weight-bearing areas) in normal cartilage or the degree of damage (normal-like, fibrillated, and ulcerated) in osteoarthrotic articular cartilage. In the latter tissue the increased synthetic capacity of the cells seems to be a diffuse rather than a localised process, for it was also found in cartilage from peripheral osteophytes. Histo-autoradiographic studies showed that the osteoarthrotic chondrocytes are metabolically hyperactive all over the femoral head, including wedge-shaped margins of the zone of exposed bone. These results support the hypothesis that much of the articular cartilage from osteoarthrotic femoral heads is of an immature chondroblastic type. It is suggested that de-novo synthesis of articular cartilage occurs during the process of regional remodelling of the femoral head, which would account for the observed hyperactivity.

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Identification and concentration of the glycosaminoglycans of human articular cartilage in relation to age and osteoarthritis

Cited by 66 publications

References 37 publications

Chemical composition and swelling of normal and osteoarthrotic femoral head cartilage. I. Chemical composition.

Chemical composition and swelling of normal and osteoarthrotic femoral head cartilage. I. Chemical composition.

Pathogenesis of Degenerative Joint Disease in the Human Temporomandibular Joint

Metabolism of human femoral head cartilage in osteoarthrosis and subcapital fracture.

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