Early childhood caries affects 28% of children aged 2–6 in the US and is not decreasing. There is a well-recognized need to identify susceptible children at birth. Caries-free adults neutralize bacterial acids in dental biofilms better than adults with severe caries. Saliva contains acidic and basic proline-rich proteins (PRPs) which attach to oral streptococci. The PRPs are encoded within a small region of chromosome 12. An acidic PRP allele (Db) protects Caucasian children from caries but is more common in African Americans. Some basic PRP allelic phenotypes have a three-fold greater frequency in caries-free adults than in those with severe caries. Early childhood caries may associate with an absence of certain basic PRP alleles which bind oral streptococci, neutralize biofilm acids, and are in linkage disequilibrium with Db in Caucasians. The encoding of basic PRP alleles is updated and a new technology for genotyping them is described.

Background: Dental biofilms contain a protein that inhibits mammalian cell growth, possibly lysine decarboxylase from Eikenella corrodens. This enzyme decarboxylates lysine, an essential amino acid for dentally attached cell turnover in gingival sulci. Lysine depletion may stop this turnover, impairing the barrier to bacterial compounds. The aims of this study are to determine biofilm lysine and cadaverine contents before oral hygiene restriction (OHR) and their association with plaque index (PI) and gingival crevicular fluid (GCF) after OHR for 1 week.Methods: Laser‐induced fluorescence after capillary electrophoresis was used to determine lysine and cadaverine contents in dental biofilm, tongue biofilm, and saliva before OHR and in dental biofilm after OHR.Results: Before OHR, lysine and cadaverine contents of dental biofilm were similar and 10‐fold greater than in saliva or tongue biofilm. After 1 week of OHR, the biofilm content of cadaverine increased and that of lysine decreased, consistent with greater biofilm lysine decarboxylase activity. Regression indicated that PI and GCF exudation were positively related to biofilm lysine after OHR, unless biofilm lysine exceeded the minimal blood plasma content, in which case PI was further increased but GCF exudation was reduced.Conclusions: After OHR, lysine decarboxylase activity seems to determine biofilm lysine content and biofilm accumulation. When biofilm lysine exceeds minimal blood plasma content after OHR, less GCF appeared despite more biofilm. Lysine appears important for biofilm accumulation and the epithelial barrier to bacterial proinflammatory agents. Inhibiting lysine decarboxylase may retard the increased GCF exudation required for microbial development and gingivitis.

Background: Lysine, a nutritionally essential amino acid, enters the oral cavity in gingival crevicular fluid (GCF). During oral hygiene restriction (OHR), lysine decarboxylase (LDC) in dento‐gingival biofilms converts lysine to cadaverine. Lysine depletion impairs the dental epithelial barrier to bacterial proinflammatory products. Antibodies to LDC from Eikenella corrodens (Ecor‐LDC) inhibit LDC activity and retard gingival inflammation in beagle dogs. Whether E. corrodens is the major source of LDC in dental biofilms and whether the lysine analog tranexamic acid (TA) inhibits LDC activity, biofilm accumulation, and GCF exudation in a human gingivitis model were examined.Methods: Antibodies raised in goats to LDC‐rich extracts from E. corrodens cell surfaces were used to inhibit Ecor‐LDC and detect it in biofilm extracts using Western blots. Ecor‐LDC activity was measured at pH 4.0 to 11.0 and its TA dissociation constant (Ki) at pH 7.0. Young adults used a 5% or 10% TA mouthwash three times daily during OHR for 1 week.Results: Ecor‐LDC antibodies and TA inhibited biofilm LDC. Ki of TA for Ecor‐LDC was 940 μM. TA reduced plaque index (PI) by downshifting the PI correlation with biofilm lysine content after OHR without TA. GCF was correspondingly suppressed. However, greater TA retention in saliva partially relieved GCF suppression but not biofilm lysine depletion.Conclusions: TA slightly inhibits LDC but strongly reduces biofilm by inhibiting bacterial lysine uptake. Unfortunately, TA may impair dental epithelial attachments by also inhibiting lysine transporter uptake. Ecor‐LDC inhibitors other than lysine analogs may maintain sufficient lysine levels and attachment integrity to prevent periodontal inflammation.

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.