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.

Highlights

  • Overview of Inflammatory Periodontal and Intestinal Diseases1.1

  • We have discovered that gingivitis is initiated and maintained by lysine decarboxylase from Eikenella corrodens (LdcE), an enzyme that converts lysine to cadaverine and carbon dioxide [2]

  • Multivariate analyses indicated that cadaverine in saliva was primarily associated with a higher periodontally inflamed surface area (PISA), whereas salivary metabolites that decreased after debridement included those associated with butyrate metabolism and lysine degradation [95]

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Summary

Roles of Cadaverine and Butyrate

The teeth lie in alveolar bone surrounded by the periodontium, which consists of the gingiva and periodontal membrane, both composed of many large bundles of fibrous collagen surrounded by small amounts of elastic (oxytalan) fibers and other connective tissue proteins. Persistent gingivitis and cadaverine protect the biofilm microbiome and change its composition into one that synthesizes butyrate and mediates periodontitis [3,4,5]. A paradox is that the same combination of bacterial products, cadaverine and butyrate, maintain a commensal (probiotic) microbiome in the intestine. Med. 2021, 10, 2360 roles and initiating factors of cadaverine and butyrate production in periodontal of and intestinal diseases. Oxygen access decreases, and the biofilm microbiome increases especially because GCF is a better bacterial substrate than saliva. Effective oral hygiene removes the butyrate, the dysbiotic biofilm, and the acids to butyrate, which activates tissue destruction (periodontitis).

Progression of Gingivitis to Periodontitis
Illustrations
The Healthy Dental Epithelial Attachment
Discovery of Ldc and Butyrate in Dentogingival Biofilms
Ldc Structure and Activity in Dentogingival and Intestinal Biofilms
The Commensal and Dysbiotic Dentogingival Biofilm Microbiome
Lysine Degradation in Gingivitis and Periodontitis
Butyrate Induces Periodontitis
2.10. Butyrate-Producing Bacterial Pathways
2.11. Cadaverine and Butyrate after Periodontal Therapy
Butyrate Paradox Resolved
Immunological Association of IBD with Periodontal Disease
Periodontal Disease
Interactions with Other Chronic Inflammatory Diseases
Findings
General Conclusions
Full Text
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