Resolving the Contradictory Functions of Lysine Decarboxylase and Butyrate in Periodontal and Intestinal Diseases

Abstract

Periodontal disease is a common, bacterially mediated health problem worldwide. Mastication (chewing) repeatedly traumatizes the gingiva and periodontium, causing traces of inflammatory exudate, gingival crevicular fluid (GCF), to appear in crevices between the teeth and gingiva. Inadequate tooth cleaning causes a dentally adherent microbial biofilm composed of commensal salivary bacteria to appear around these crevices where many bacteria grow better on GCF than in saliva. We reported that lysine decarboxylase (Ldc) from Eikenella corrodens depletes the GCF of lysine by converting it to cadaverine and carbon dioxide. Lysine is an amino acid essential for the integrity and continuous renewal of dentally attached epithelium acting as a barrier to microbial products. Unless removed regularly by oral hygiene, bacterial products invade the lysine-deprived dental attachment where they stimulate inflammation that enhances GCF exudation. Cadaverine increases and supports the development of a butyrate-producing microbiome that utilizes the increased GCF substrates to slowly destroy the periodontium (dysbiosis). A long-standing paradox is that acid-induced Ldc and butyrate production support a commensal (probiotic) microbiome in the intestine. Here, we describe how the different physiologies of the respective tissues explain how the different Ldc and butyrate functions impact the progression and control of these two chronic diseases.

Combined assessment of Lysine and N-acetyl cadaverine levels assist as a potential biomarker of the smoker periodontitis

“…The N1, N8-diacetyl spermidine, and N-acetyl cadaverine levels showed highly signi cant increase in periodontitis with smoker and reverse smoker groups which was similar to previously reported (Goldberg et al, 1994). Elevated levels of lysine in the present study correlated with the study that showed conversion of lysine to cadaverine promotes gingivitis, and lysine depletion promotes gingivitis and periodontitis (Levine & Lohinai, 2021). The failure of GCF exudation in smokers results in the junctional epithelial attachment becoming deprived of amino acids including lysine.…”

“…The failure of GCF exudation in smokers results in the junctional epithelial attachment becoming deprived of amino acids including lysine. The increase in N acetylcadaverine is tightly associated as putative component of oral malodor and butyrate producing microbiome which lead to enhanced GCF substrate and slowly destroy the periodontium (Goldberg et al, 1994;Levine & Lohinai, 2021).…”

“…Salivary cadaverine and its derivative, N-acetyl cadavrine were higher in periodontal in amed surface area which lead to enhanced gingival cervical uid (GCF). This helped in slow destruction of the periodontium (Goldberg et al, 1994;Levine &Lohinai, 2021 andSakanaka et al, 2017). As the periodontitis disease characteristics match with the multiple roles played by PA, this study aimed to analyze and check for differences in PA levels among periodontally and systemically healthy, nonsmokers, smokers, and reverse smokers with periodontitis.…”

Gut Microbial Metabolite Butyrate and Its Therapeutic Role in Inflammatory Bowel Disease: A Literature Review

“…Gut microbiota produces butyrate from acetyl-CoA, lysine, glutarate, or succinate pathways in the colon [ 21 ]. Various bacterial species in the human intestine generate enzymes that can synthesize butyrate from complex fermentable substrates.…”

Gut Microbial Metabolite Butyrate and its Therapeutic Role in Inflammatory Bowel Disease

“…Butyrate, a four-carbon SCFA, is one of the major energy sources for intestinal epithelial cells. Gut microbiota produces butyrate from acetyl-CoA, lysine, glutarate, or succinate pathways in the colon [20]. Various bacterial species in the human intestine generate enzymes that can synthesize butyrate from complex fermentable substrates.…”