Bad Breath has a variety of etiologic factors

Bad Breath has a variety of etiologic factors

Author: Aila R. Cruvinel

The etiology of oral malodor is multifactorial. In the presence of adequate substrate with appropriate conditions, a sequence of events leads to the release into the oral cavity of pungent gases that pollute exhaled air and are perceived as bad breath. Research has identified several microorganisms that produce these offensive odors and provided a fair explanation of the conditions necessary for their production. In addition to the presence of certain types of bacteria, the type and amount of substrate, and oxygen and pH levels influence the occurrence and severity of oral malodor.

Certain chemical end products of bacterial putrefaction known as volatile sulfur compounds (VSCs) are foul smelling and determined to be responsible for the offensive odor recognized as bad breath.l2-l5 Nonsulfur-containing compounds such as cadaverine, putrescine, indole and skatolel6,l7 have also been implicated in the foul smell of oral malodor, but their contribution is thought to be limited.7 VSCs such as hydrogen sulfide, methyl mercaptan, dimethyl sulfide and dimethyl disulfide make up more than 90 percent of the putrid odors from the mouth.8 Two of these VSCs, hydrogen sulfide and methyl mercaptan, account for approximately 90 percent of the total VSCs identified with putrid odors from the mouth.9,l8

Specific groups of bacteria have been identified with the production of oral malodor. Using in vitro methods, McNamara and colleagues demonstrated that the formation of putrid odors from incubated saliva correlated with a shift in the microbial flora from a predominately gram-positive to a predominately gram-negative anaerobic flora.6 Concomitant with this shift in flora, they observed a depletion of carbohydrates and a rise in the pH level of the stagnant saliva. As the carbohydrates are depleted, the gram-positive acidogenic flora are suppressed and the gram-negative microorganisms, capable of protein metabolism, become progressively more dominant.7 Evaluated individually, none (n=9) of the gram-positive microorganisms produced an unpleasant odor whereas all (n=4) of the gram-negative microorganisms (Fusobacterium polymorphum, Veillonella alcalescens, Bacteroides fundiliformis, Klebsiella pneumoniae) produced a putrid odor.6 In a similar study, Solis-Gaffar and colleagues found that only the gram-negative microorganisms (Veillonella alcalescens, Fusobacterium nucleatum, Bacteroides melanogenicus and Klebsiella pneumoniae) produced VSCs.l9The production of VSCs was accompanied by an unpleasant odor and a rise in the pH level of the saliva mixture. Except for Klebsiella pneumoniae, all gram-negative microorganisms required blood in the mixture to produce VSCs. None (n=8) of the gram-positive microorganisms produced VSCs with or without blood products.l9

Anaerobic conditions, necessary for the production of VSCs, are created in microenvironments. The accumulation of plaque and debris and the stagnation of saliva occur most commonly in areas where tooth and tissue crevices lend themselves to stagnant microenvironments. The most common sites for stagnation, plaque accumulation and production of VSCs are the posterior dorsum tongue, interdental spaces and subgingival areas.l7 Dental plaque progresses from an aerobic, gram-positive colonization to one that is anaerobic, favoring gram-negative growth. As the bacterial plaque matures (0.1-0.2 mm thickness), the oxygen level drops to zero, favoring reduced conditions and the production of odoriferous volatiles.20 Oxygen depletion is attributed to the bacteria that use oxygen to oxidize substrates. Anaerobic bacteria produce foul-smelling VSCs from the sulfur-containing proteins and amino acids found in saliva and crevicular fluid.ll,2l Putrefactive formation of VSCs is favored by an alkaline pH (7.2) and inhibited by an acidic pH (6.5).7 The presence of glucose (0.02 M) also inhibits the formation of VSCs7

Specific sulfur-containing precursors are required for the bacterial production of VSCs. Proteinaceous substrates�namely exfoliated epithelium, leukocytes, food debris and dead bacteria�are degraded by proteolysis into peptides. and amino acids. The sulfur-containing amino acids, specifically cysteine and methionine, are further degraded into VSCs. Gas chromatographic studies have identified hydrogen sulfide and methyl mercaptan as the putrefactive end products of cysteine and methionine, respectively.22 Exfoliated epithelial cells and effused leukocytes are the major sources of protein with sulfur-containing amino acids.7,9,27 The severity of oral malodor (VSC level) is influenced by bacterial plaque levels, substrate availability, time of day and oral dryness.5 Oral malodor is worst in the morning, following an extended period of oral dryness and undisturbed bacterial putrefaction.8 Oral malodor improves following oral hygiene procedures.8 There is evidence to suggest that periodontal disease increases the severity of oral malodor.

Treatment of Oral Malodor

Oral malodor is a multifactorial problem that requires a well-defined approach to diagnosis and treatment. Successful treatment is associated with the ability to identify the major and minor contributing factors and to address them with appropriate and effective therapy. When periodontitis, pathologically deep pockets or heavy deposits are identified in an individual with chronic halitosis, treatment of the periodontal disease and improved oral hygiene can produce excellent clinical outcomes.7 Numerous oral hygiene devices and chemical agents can be implemented to improve plaque control and thus effectively manage oral malodor. Patient education about oral hygiene practices is crucial to the successful treatment of oral malodor associated with periodontitis. Periodontal pockets and defective and overhanging restorations that are difficult or impossible to clean should be treated to improve access and correct defects. The successful treatment of periodontal disease is greatly dependent on the patient's daily practice of good oral hygiene to control bacterial plaque growth and progression. Likewise, the successful treatment of oral malodor is greatly dependent on personal oral hygiene.

�Clinical examination for signs and symptoms of periodontal disease remains the most common method for detection of gingivitis and periodontitis. Observation for clinical signs of erythema in the gingiva are diagnostic for current periodontal inflammation. Measuring probing pocket depths with a periodontal probe detects previous attachment loss, calculus deposits and periodontal pocket formation. Although not predictive of future periodontal breakdown, bleeding/exudate from the periodontal pocket or increased temperature within the pocket can indicate disease activity. Radiographic examination determines the degree of prior bone loss and helps detect areas that are inaccessible to cleaning, such as overhangs, caries and furcations. A diagnosis of periodontitis would lead to a series of steps including oral hygiene instructions (D) specifically directed at the periodontal condition and plaque control, periodontal therapy (E) for pocket reduction, plaque control and calculus removal followed by a re-evaluation (F) to determine disease control. Any poor restorations, overhangs or caries should also be treated and/or corrected. The specific contribution of bacterial pathogens to the oral malodor can be assessed in selected cases via indirect methods such as BANA hydrolysis. (G) However, the BANA hydrolysis test is an indirect measure used to determine the presence of the periodontal pathogenic microorganisms. As mentioned above, these tests do not measure the offending compounds.

The ultimate goal of treatment for oral malodor should be directed at eliminating or at least reducing the causative microorganisms and associated substrates. If the microorganisms' quantity and plaque maturity are controlled, then their capabilities to produce VSCs is greatly reduced. The substrate available for metabolic breakdown should likewise be eliminated or reduced with good oral hygiene and control of periodontal inflammatory disease.

Conclusion

An estimated 80 percent to 90 percent of all bad breath odors originate from the mouth and are caused by bacteria. Anaerobic bacteria, oxygen depletion, alkaline pH and sulfur-containing substrates are some of the requirements for oral malodor to occur. The accumulation of plaque and debris and the stagnation of saliva occur most commonly in areas where tooth and tissue crevices lend themselves to stagnant microenvironments. The most common sites for the production of VSCs (hydrogen sulfide and methyl mercaptan) are the posterior dorsum tongue, interdental spaces and subgingival areas.

The association among periodontal pathogenic microorganisms, periodontal disease and oral malodor has been strongly implicated but not proved. Although oral malodor is probably not caused by periodontal disease, there is ample evidence to suggest that periodontal disease increases the severity of oral malodor. Periodontitis worsens the severity of oral malodor by providing additional sites of VSC production (interdental and subgingival), an increased availability of sulfur-containing substrate (exfoliated epithelial cells and leukocytes) and an increased rate of methionine metabolism (precursor to methyl mercaptan). Periodontitis contributes to an increased tongue coating with higher VSC production. There is evidence to suggest that VSCs, i.e., oral malodor, may contribute to the progression and pathogenesis of periodontal disease via increased mucosal permeability. Treatment for oral malodor should be directed at eliminating or at least reducing the causative microorganisms and the associated substrates with diligent oral hygiene procedures. It is essential to diag nose and control any periodontal disease that may coexist and worsen the severity of oral malodor.

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