Stimulation of enzyme and cytokine production by methyl mercaptan in human gingival fibroblast and monocyte cell cultures

Ratkay, Leslie G.; Waterfield, J D; Tonzetich, J.

doi:10.1016/0003-9969(94)00165-8

Cited by 46 publications

(33 citation statements)

References 49 publications

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“…26,35,36 These compounds increase cathepsin B and cAMP, secretion of PGE 2 , and permeability of the oral mucosa, decrease protein and collagen synthesis, and inhibit growth and proliferation of epithelial cells. [37][38][39][40][41] It has also been shown that exposure to methyl mercaptan alters protein synthesis in human gingival fibroblasts, inhibits cell migration, and reduces intracellular pH in periodontal ligament cells. 42,43 On the basis of a previous report, 30 it seems that most strains of H. pylori require sulfur-containing amino acids and can produce VSCs.…”

Section: Discussionmentioning

confidence: 98%

Volatile Sulfur Compounds Produced by Helicobacter pylori

Lee

Kho

Chung

et al. 2006

Journal of Clinical Gastroenterology

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Section: Discussionmentioning

confidence: 98%

Volatile Sulfur Compounds Produced by Helicobacter pylori

Lee

Kho

Chung

et al. 2006

Journal of Clinical Gastroenterology

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“…Methyl mercaptan has also been shown to induce interleukin-1␤ secretion from mononuclear cells (19). To evaluate whether the mgl gene is associated with the pathogenicity of P. gingivalis, the virulence of the parent strain W83 and the mgl-deficient mutant M1217 was tested in a mouse abscess model.…”

Section: Discussionmentioning

confidence: 99%

Formation of Methyl Mercaptan from l -Methionine by Porphyromonas gingivalis

et al. 2000

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Methyl mercaptan production by oral bacteria is thought to be one of the main causes of oral malodor. We examined the ability of periodontopathic Porphyromonas gingivalis to produce methyl mercaptan from L-methionine and found that the invasive strains W83 and W50 produced large amounts of methyl mercaptan. We cloned and sequenced the mgl gene encoding L-methionine-␣-deamino-␥-mercaptomethane-lyase (METase) from P. gingivalis W83. The structural mgl gene consisted of 1,200 bp and encoded a 43.3-kDa protein. To examine the role of methyl mercaptan in the pathogenesis of P. gingivalis, a METase-deficient mutant of P. gingivalis W83 was constructed. The methionine degradation activity and virulence of the mutant (M1217) and the parent strain (W83) in mice were compared. M1217 showed a marked decrease in the formation of methyl mercaptan from L-methionine and decreased virulence compared with the wild-type strain W83. These results suggest that methyl mercaptan not only is one of the sources of oral malodor, but may also play a role in the pathogenicity of P. gingivalis.Oral malodor is caused mainly by volatile sulfur compounds (VSCs), such as hydrogen sulfide, methyl mercaptan, and dimethyl sulfide (21). Of these VSCs, hydrogen sulfide and methyl mercaptan are predominant in mouth air. Both compounds are highly toxic, especially methyl mercaptan (21). VSCs can increase the permeability of the oral mucosa (16) and decrease protein or collagen synthesis (6,8). It is possible that the presence of methyl mercaptan within a periodontal pocket is involved in the induction or progression of periodontal disease. Coil et al. (2) reported that the increase in the ratio of methyl mercaptan to hydrogen sulfide in human gingival crevicular sites is correlated with deeper pockets or bleeding pockets. Exposure to methyl mercaptan alters protein synthesis in human gingival fibroblasts (7) and inhibits cell migration in periodontal ligament cells (11). These findings suggest that methyl mercaptan not only may be responsible for oral malodor but also may contribute to the pathogenesis of periodontal disease.Methyl mercaptan is produced from L-methionine by the enzymatic action of L-methionine-␣-deamino-␥-mercaptomethane-lyase (METase), which catalyzes the ␣,␥ elimination of L-methionine to produce ␣-ketobutyrate, methyl mercaptan, and ammonia. This enzyme is detected in anaerobic, nonoral microorganisms, such as Pseudomonas, Trichomonas, and Clostridium (4, 5, 9, 13). In addition, Porphyromonas gingivalis, a black-pigmented anaerobe, which is implicated as a major pathogen in adult periodontitis, is known to produce large amounts of methyl mercaptan in human serum (18). However, little is known about P. gingivalis METase and the role of methyl mercaptan in the pathogenesis of this organism. In this study, we cloned the mgl gene homolog encoding METase from the virulent strain P. gingivalis W83 and confirmed its nucleotide sequence. To determine the role of METase in the pathogenicity of P. gingivalis, we constructed a METase-defici...

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“…23,24 The collagen content of gingival connective tissue decreases dramatically in periodontal disease. 14,15 Methyl mercaptan has also been shown to induce interleukin-1 beta (IL-1 β) from mononuclear cells and act synergistically with both IL-1 β and LPS resulting in an increase of prostaglandin E2 and collagenase, both of which are important mediators of inflammation and tissue destruction.…”

Section: Figurementioning

confidence: 99%

The Negative Effects of Volatile Sulphur Compounds

Milella¹

2015

J Vet Dent

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Oral malodor has been studied extensively in humans but not necessarily to the same degree in our veterinary patients where malodor constitutes a significant problem. Breath malodor may originate from the mouth, or from an extra oral source, originating from other organ systems such as gastrointestinal, respiratory, or even systemic disease. Oral malodor is a result of microbial metabolism of exogenous and endogenous proteinaceous substrates leading to the production of compounds such as indole, skatole, tyramine, cadaverine, puterescine, mercaptans, and sulphides. Volatile sulphur compounds have been shown to be the main cause of oral malodor. Although most clients perceive oral malodor to be primarily a cosmetic problem, there is an increasing volume of evidence in human dental literature demonstrating that volatile sulphur compounds produced by bacteria, even at low concentrations, are toxic to tissues and play a role in the pathogenesis of periodontitis. This article reviews the current available literature in human dentistry looking at these negative effects. No veterinary studies have been conducted looking at the negative effects of volatile sulphur compounds specifically, but as this article highlights, we should be aware of the potential negative effects of volatile sulphur compounds and consider this an area of future research.

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Stimulation of enzyme and cytokine production by methyl mercaptan in human gingival fibroblast and monocyte cell cultures

Cited by 46 publications

References 49 publications

Volatile Sulfur Compounds Produced by Helicobacter pylori

Volatile Sulfur Compounds Produced by Helicobacter pylori

Formation of Methyl Mercaptan from l -Methionine by Porphyromonas gingivalis

The Negative Effects of Volatile Sulphur Compounds

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