Glucocorticoid inhibition of glycosaminoglycan biosynthesis: Decrease of protein acceptor

Elders, M. Joycelyn; McNatt, M; Kilgore, B S; Hughes, Edwin R.

doi:10.1016/s0006-291x(77)80015-6

Cited by 7 publications

(3 citation statements)

References 18 publications

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“…The reduced incorporation of 35 SO4 into differentiating cartilage could be due to several reasons: 1) decreased proliferation and/ or maturation of cartilage progenitor cells, 2) decreased transport of 35 SO 4 into chondrocytes, causing a reduction in the incorporation of radioactivity, or 3) direct interference with proteoglycan biosynthetic mechanisms. In this context, it is known that corticosteroids in many instances reduce cellular permeability and bring about membrane stabilization (21)(22)(23) and also interfere with biosynthesis of glycosaminoglycans through a possible interference with the synthesis of the protein core (24).…”

Section: Discussionmentioning

confidence: 99%

Influence of Adrenalectomy and Dexamethasone on Matrix-Induced Endochondral Bone Differentiation

Rath

Reddi

1979

Endocrinology

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Effects of adrenalectomy and corticosteroid treatment on the temporal aspects of matrix-induced endochondral bone differentiation were examined using various biochemical parameters at discrete stages of development. In our previous study, we demonstrated a peak of ornithine decarboxylase (ODC) on day 3 concomitant with extensive proliferation of mesenchymal cells. Administration of corticosteroids, particularly dexamethasone, on days 0 and 1 or their implantation with bone matrix inhibited the increase in ODC activity, in contrast to other steroid hormones tested. Conversely, adrenalectomy increased the ODC activity over normal levels. Dexamethasone diminished the incorporation of 35 SO4 into proteoglycans of the plaques during chondrogenesis on day 7, whereas adrenalectomy had no marked influence on this process. Dexamethasone treatment from days 7-10 impaired osteogenesis and mineralization, whereas treatment on days 10 and 11 did not affect osteogenesis and mineralization, as indicated by the levels of alkaline phosphatase and incorporation of 45 Ca in plaques of days 11 and 12, respectively. However, in the latter group, the level of alkaline phosphatase was elevated in response to dexamethasone treatment. These results indicate that the action of corticosteroids on differentiation of endochondral bone may be mediated primarily through their influence on proliferation of mesenchymal cells before chondrogenesis and osteogenesis. (Endocrinology

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Section: Discussionmentioning

confidence: 99%

Influence of Adrenalectomy and Dexamethasone on Matrix-Induced Endochondral Bone Differentiation

Rath

Reddi

1979

Endocrinology

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“…The ability of corticosteroid hormones to inter-ber of osteocytes in femoral heads and showed fere with the host defence mechanism against signs of avascular necrosis in the bone. Ininfection is well documented (for general ref-creased serum levels of corticosteroid hormones erence see Thomas 1953, Katler & Weissmann have also been associated with osteoporosis in 1977), but corticosteroid hormones also in-man and in laboratory animals (Applebaum & fluence e.g, the metabolic activity of fibroblasts Seelig 1955, Caniggia & Gennari 1973, (Pratt & Aronow 1966, Berliner & Nabors 1967 The potential of corticosteroid hormones to Elders et al 1977, Saarni et al 1978, and influence the inflammatory reaction and host decrease the synthesis of both collagen and defence against infection in general suggests matrix components (Kivirikko 1963, Dietrich et that long-term administration of such horal. 1979), mones may interfere with the development and Fisher et al, (1971Fisher et al, ( , 1972 and Cruess et al, progression of plaque-associated gingivitis and (1975) reported that, in comparison to normal periodontal disease (Waterhouse 1969), From controls, patients who had been on systemic experiments in animals and observations in corticosteroid therapy following kidney trans-humans, it has been suggested that the adminiplantation appeared to have a diminished num-stration of corticosteroids may result in an increased osteoporosis of alveolar bone (Glickman et al 1953, Glickman & Schklar 1955, Dreizen et al 1971), a reduced number of osteoblasts and decreased bone tissue formation (Labelle & Schaffer 1967).…”

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confidence: 99%

Corticosteroid therapy and periodontal disease

Safkan

Knuuttila

1984

J Clinic Periodontology

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In the present investigation, the frequency and severity of periodontal disease was assessed in a group of patients with multiple sclerosis receiving corticosteroid hormone therapy for neurological disease. Age-matched patients with multiple sclerosis but without hormone therapy as well as healthy subjects served as controls. Individuals suffering from multiple sclerosis or polyneuropathies were selected from a pool of patients who were under treatment at the Department of Neurology, The Central Hospital of Kuopio, Finland. 27 individuals were identified who had received more than 1.5 g prednisone over a 1-4 year period. The average amount of steroid given to these patients was 3.5 g. 26 individuals also suffering from neurologic disease had received no or only negligable amounts of hormone therapy and were used as diseased controls. Another control group comprised age- and sex-matched healthy individuals from the city of Kuopio. The dental examination which was performed by one dentist comprised assessments of the following parameters: oral hygiene status, gingival conditions, probing depth, gingival recession and height of the alveolar bone. The findings clearly demonstrated that patients with neurological disease who received corticosteroid therapy had the same frequency of gingivitis as non-treated diseased controls. Furthermore, data describing probing depth, gingival recession and height of the alveolar bone revealed that there was no difference regarding the frequency and severity of periodontal disease between the 2 groups of neurological diseased patients. It was concluded that corticosteroid therapy maintained over 1-4 years had no obvious influence on clinical parameters of periodontal disease in patients suffering from neurological disease.

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“…This is in contrast to a recent report (FAROOQUI et al, 1977) which claimed that treatment of neuroblastoma and astrocytoma cells for 2 4 days with cortisol induced both morphological changes and a 4-fold elevation in arylsulfatase A, B and b-galactosidase activities. Previous in uivo studies have shown that cortisol and related corticosteroids inhibit glycosaminoglycan synthesis (SCHILLER & DORF-MAN, 1957;ELDERS et al, 1977) although the effect may be at the core protein rather than the sulfation level. Almost all tissue culture media is supplemented with at least 10% animal serum and such sera contains corticosteroids bound to transcortin.…”

Section: Discussionmentioning

confidence: 99%

Induction of sulfogalactosylceramide (sulfatide) synthesis by hydrocortisone (cortisol) in mouse G‐26 oligodendroglioma cell strains

Dawson¹,

Kernes

1978

Journal of Neurochemistry

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Glucocorticoid inhibition of glycosaminoglycan biosynthesis: Decrease of protein acceptor

Cited by 7 publications

References 18 publications

Influence of Adrenalectomy and Dexamethasone on Matrix-Induced Endochondral Bone Differentiation

Influence of Adrenalectomy and Dexamethasone on Matrix-Induced Endochondral Bone Differentiation

Corticosteroid therapy and periodontal disease

Induction of sulfogalactosylceramide (sulfatide) synthesis by hydrocortisone (cortisol) in mouse G‐26 oligodendroglioma cell strains

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