Relationship of Periodontal Disease to Oral Malodor - Periodontics NY

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Patients with chronic periodontitis and pocket formation frequently suffer from unpleasant mouth odor associated with accumulated debris and an increased rate of putrefaction.8,l0,ll,14,l5,23,24 The fetid odor characteristic of acute necrotizing ulcerative gingivitis is an extreme example of malodor from periodontal pathogens.25 Periodontal conditions that favor the bacterial growth and retention of debris contribute to oral malodor. Interproximal spaces and periodontal pockets are conducive to anaerobic growth and microenvironments for the production of VSCs. These subgingival and interproximal periodontal malodors make a significant contribution to overall oral malodor.26,27

In an evaluation of oral malodor in healthy subjects and patients with periodontal disease, Yaegaki and Sanada found that bleeding on probing and periodontal pocket depth positively correlated with the production of VSCs.l5 Deep periodontal pockets (3-5mm) were more likely to harbor and promote the growth of VSC-producing microorganisms. Samples of interdental plaque, obtained with dental floss, demonstrate the production of offensive VSCs.28,29 VSCs, specifically hydrogen sulfide and methyl mercaptan, have been identified in patients with gingivitis and periodontitis.l0,l2,30 In fact, a positive correlation has been reported between the amounts of hydrogen sulfide produced and the depth of periodontal pockets.31 An increase in production of VSCs from periodontal pockets provides a plausible explanation for the intensification of oral malodor observed in patients with periodontal disease.

Periodontal pathogens have been positively correlated with oral malodor.ll-l5 Several periodontal pathogens including Treponema denticola, Porphymonas gingivalis and Bactericides forsythias have been identified, with BANA hydrolysis, on the posterior tongue, contributing to oral malodor.13,32,33 Additional periodontal pathogens, including Fusobacterium nucleatum and Bacteroides melanogenicus have been identified as VSC formers.8,19 These microorganisms produce copious amounts of hydrogen sulfide, methyl mercaptan and dimethyl disulphide.

Several studies suggest that periodontitis increases the severity of oral malodor.7 One possible explanation is the increased amount of substrate available to be metabolized. In patients with periodontitis, more sulfur-containing protein substrate is available through increased exfoliation of epithelial cells and crevicular effusion of leukocytes.7 Sato and colleagues found that the number of leukocytes increased in the saliva of patients with periodontitis and that the level of methyl mercaptan produced correlated with bleeding on probing,, pocket depth and gingival exudate.23 In another study, the metabolism of methionine to methyl mercaptan was found to be significantly higher in the saliva of patients with periodontitis.11 Together, these findings suggest that inflamed periodontal tissues provide more methionine, which is converted into methyl mercaptan at a higher rate than for healthy gingival tissues. Indeed, methyl mercaptan contributes significantly to the oral malador in patients with periodontal disease.35 The concentration of methyl mercaptan in mouth air correlated with the severity of periodontal disease. The increased gingival crevicular fluid flow in periodontitis may be a continual source of methionine.11

Bacterial samples from the tongue in individuals with severe oral malodor were consistently found to be positive for BANA hydrolysis.l3~33 Subjects with higher oral malodor (organoleptic measurements) and VSC scores had more positive BANA hydrolysis and bleeding on probing than individuals with low scores, suggesting that peri-odontal pathogens and the coexistence of periodontitis played a significant role in those individuals with severe oral malodor.13 The average amount of tongue coating in patients with periodontal disease was six times greater than the amount in healthy indi-viduals.15 The estimated production of VSC from the tongue coating was four times greater in individuals with periodontal dis-ease.1l~ls The greater tongue coating in these periodontal patients comprises ep-ithelial cells, leukocytes and microorganisms released from peri-odontal pockets.11

In contrast to the view that periodontal disease contributes to oral malodor, Bosy and colleagues found that oral hygiene levels and not periodontal pockets were more indicative of oral malodor,36 which supports the concept that oral malodor may be an independent entity. Certainly, some gram-negative anaerobic bacteria, which are not known to be periodontal pathogens (Fusobacterium polymorphum, Veillonella alcalescens, Bacteroides fundiliformis and Klebsiella pneumoniae) have been identified with oral malodor.6,19 The bacteria contributing to oral malodor in healthy individuals are most commonly located on the posterior dorsal tongue surface as opposed to in periodontal locations.17

In addition to being a major contributor to oral malodor, VSCs have been implicated in the disruption of oral mucosa and may contribute to the progression of periodontal disease.37 As currently understood, periodontal disease progression consists of a shift in the bacterial plaque from a gram-positive aerobic flora to a gram-negative anaerobic and motile flora. Some studies suggest that the production of VSCs by these microorganisms may contribute to the progression of periodontal disease via breakdown of the oral mucosa leading to bacterial invasion.38 Ng and Tonzetich found that the permeability of porcine sublingual mucosa increased 75 percent and 103 percent following exposure to hydrogen sulfide and methyl mercaptan, respectively.37 This finding suggests that the VSCs of oral malodor could contribute to the pathogenesis periodontists.

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