RATIONALE FOR PLAQUE CONTROL

The rationale for controlling periodontal conditions by regular plaque removal is based on the premise that supragingival plaque, if undisturbed, will become subgingival plaque,⁹² and subgingival plaque has the potential to be colonized by periodontopathogenic bacteria. Although relatively few gingivitis sites progress to periodontitis (see Chapter 21), we still cannot identify those sites that will. Accordingly, the principle for prevention has not changed for years: the regular and consistent control of plaque buildup, supragingival and subgingival, soft and mineralized (calculus), on the teeth and in the gingival crevices. This approach is bacteriologically nonspecific, for it seeks to control the buildup of all plaque. It also depends strongly on individual motivation for success. Plaque control is therefore unlikely ever to be completely effective in preventing periodontal diseases in a population, although individual success is common. Until research produces methods of controlling periodontal infection, enhancing host response, and identifying susceptible individuals, however, mass plaque control by personal, professional, or chemical means is the best we can do.

This chapter deals with methods for controlling the deposition of dental plaque, an approach that can effectively prevent gingivitis. As was detailed in Chapter 21, however, the role of plaque in periodontitis is not so straightforward. Plaque deposits may be a necessary condition for periodontitis, but clearly they are not sufficient. In other words, susceptible people may have to be stringent about oral hygiene, but there are millions of people with poor oral hygiene who do not have serious periodontitis. There is an analogy here with the role of consumption of sugars in the development of caries: caries-susceptible persons have to restrict their intake of sugars, but there are many people who consume a lot of sugars but have little or no caries as a consequence.

NATURE OF DENTAL PLAQUE

Although dental plaque is commonly depicted as the root cause of both caries and periodontitis, one should remember that it must have evolved in humans for some purpose. Commercial advertising would have us believe that oral health depends on the complete removal of all plaque at all times, but clearly that is not only not possible but also not desirable. Dental plaque forms naturally on the teeth and benefits the host by helping to prevent intraoral colonization by exogenous species.⁸⁸ Plaque’s role in promoting remineralization of demineralized lesions was described in Chapter 20.

Dental plaque is a natural biofilm that forms on the tooth surface and consists of a diverse microbial community embedded in a polymer matrix of bacterial and salivary origin.⁸⁹ After a tooth surface is cleaned, the pellicle, a conditioning film of proteins and glycoproteins, is adsorbed rapidly onto the tooth surface. The interactions between pellicle and early bacterial colonizers are the first steps in plaque formation. Secondary bacterial colonizers adhere to these early colonizers through specific molecular interactions, a process that contributes to the pattern of bacterial succession. The biofilm character of plaque allows the survival of a diverse bacterial flora.²⁴ Although microbial adhesion is how plaque formation begins, microbial multiplication is thought to be the dominant factor in the buildup of dental plaque, and the nature of this microbial proliferation is highly dependent on the local environment. Because environmental conditions vary from place to place within the oral cavity, each site with plaque represents its own distinct ecosystem, and the dominant microbial composition at the site depends on the outcome of numerous host-microbe and microbe-microbe interactions.¹⁰⁶

The clinical picture of all this activity has been well described. After plaque has been completely removed, it re-forms slowly on the supragingival tooth surface for about 3 days, and then if left undisturbed it increases rapidly to reach a maximum bulk after 7 days. The various microbial interactions actually keep the bacterial composition of plaque relatively stable, but when this homeostasis breaks down, the shifts in microbial balance can set up conditions for caries or gingivitis to begin. Plaque accumulation around the gingival margin leads to an inflammatory host response and an increased flow of gingival crevicular fluid.⁸⁸ Few bacteria can be isolated from around healthy gingival tissue, although with gingivitis there is a considerable increase in the numbers and complexity of bacteria as the lesion develops.⁹² Subgingival plaque microflora shift from being predominantly gram positive to including increased levels of anaerobic gram-negative organisms; the character of subgingival plaque is thus quite different from that of supragingival plaque. Specifically, the gram-negative anaerobes Porphyromonas gingivalis and Bacteroides forsythus in subgingival plaque have been associated with both loss of periodontal attachment and bone loss.^48,49 Frequent professional supragingival cleaning, added to good personal oral hygiene, has a beneficial effect with regard to subgingival microbiota in moderately deep pockets.^54,120 Subgingival plaque is also characterized by oral spirochetes, whose role in periodontitis is still not clear, although their presence in the subgingival plaque is seen as a marker for disease.¹¹⁸

Calculus was formerly viewed only as an “irritating factor” in the development of periodontitis⁶⁴ and did not get much research attention. Today, however, calculus is recognized as a calcified matrix that can harbor periodontopathogenic bacteria, and subgingival calculus is closely associated with gingivitis and periodontitis.³³ Therefore, the initial formation and continued presence of both supragingival and subgingival calculus are to be prevented to the extent possible. The only known method is to control the initial formation of supragingival plaque and calculus.

APPROACHES TO PLAQUE CONTROL

Because plaque has some identifiable health functions and because disease comes more from an upset in the homeostatic balance than from infection with exogenous organisms, disease prevention should be geared more toward plaque control than plaque eradication. This concept is referred to as the ecologic plaque hypothesis.⁸⁷ The goal in preventing periodontitis is to prevent fresh plaque from becoming established plaque, which permits the growth of specific periodontopathogenic bacteria,^102,123 and to prevent supragingival plaque from becoming established subgingivally.

Several approaches to plaque control can be quickly ruled out as having no scientific basis: rinsing with water and chewing a fibrous food (e.g., remove loose food debris but do not affect plaque). There is no evidence to alter the long-held view that preventive benefits cannot be achieved by changes in diet or nutrition,^74,110 although, given the importance of the host response in periodontitis and the fact that nutrition is a vital part of the immune reaction, the role of nutrition in periodontitis should continue to be studied.

Primary prevention of gingivitis requires consistent, thorough control of plaque accumulation on a lifetime basis. The rationale is to prevent plaque from reaching the stage of maturity at which gingivitis begins. Some people are capable of maintaining an adequate oral hygiene status largely by their own efforts, but many are not. The dental professional will consistently see some level of gingivitis in the latter patients and may become frustrated in the effort to eliminate gingivitis entirely. For these patients, the dental professional’s goal should be to maintain the gingivitis at as low a level as possible. As long as the lowest possible level of gingivitis can be maintained over time, subsequent loss of periodontal support is likely to be minimized. This is true for the majority of patients who are at low risk of severe periodontitis. It is less the case for those patients with aggressive periodontitis who fit the compromised host model described in Chapter 21. Prevention of disease in these patients is difficult because we do not yet have the means of influencing the deficient host response to a periodontal challenge.

As long as plaque accumulation remains supragingival, it can be controlled by mechanical or chemotherapeutic means.¹⁰¹ Once plaque becomes established subgingivally, however, the individual patient cannot remove it by self-care, and professional intervention is necessary. The goal of prevention of periodontal conditions through plaque control by the individual is to keep supragingival plaque from accumulating.

There are essentially three approaches to preventing the build-up of dental plaque, each of which is assessed in turn. They are:

MECHANICAL PLAQUE REMOVAL BY THE INDIVIDUAL

Self-care is a fundamental part of periodontal health. Unless the individual is able to maintain at least a reasonable level of oral cleanliness by regular and consistent home care, the benefits of treatment by dental professionals will be limited. Individual effort means mechanical plaque removal with a toothbrush and aids such as dental floss, an interproximal brush, and wood points.

Although individual oral hygiene practices are fundamental to the promotion of oral health, it is surprising how little is really known about such basic things as the most efficient type of toothbrush and how often the teeth should be brushed. Research studies in these areas have often been run for only short periods and with atypical populations, such as dental or dental hygiene students. Long-term effects and the validity of projecting results to the general population are thus difficult to assess.

MECHANICAL PLAQUE REMOVAL BY THE DENTAL PROFESSIONAL

Professional care is necessary to remove subgingival plaque and calculus; the patient cannot remove plaque from deep pockets. The benefits of professional plaque removal have been shown in studies of children and adults who were in reasonable periodontal health to begin with, as well as in studies of adults receiving treatment for advanced disease.