Introduction

As the focus in dental health shifts from treatment to prevention of disease, maintaining oral hygiene is gaining importance. Periodontal care is as much important as care for prevention of caries. Knowledge about basics of normal functioning and ecological balance of the microbial community with the host is essential to know pathophysiology of disease and means to prevent or treat it. Dental plaque is an indispensable component of periodontal disease. Understanding the nature of plaque provides an invaluable insight in preserving oral health.

DENTAL PLAQUE: SIMPLE yet COMPLEX

Dental plaque has been much talked and researched about in the recent decades. Disease processes are well understood now due to detailed study of microbiology of plaque. Plaque may be classified in different ways:

1. In relation to gingival margin-

• • Supragingival
  • Subgingival

2. In relation to tooth surface-
   • Attached
   • Unattached

3. In relation to disease states-
   • Health associated
   • Disease associated

Contents of plaque:

1. ORGANIC:

• Cellular matrix: it consists of bacterial cells, epithelial cells, leucocytes, macrophages.
• Extracellular matrix: bacterial products along with saliva form the extracellular matrix, which contains protein, polysaccharide and lipids.

2. INORGANIC:

• Calcium and phosphorous, which are mostly derived from saliva, and it increases as calculus develops.

SEQUENCE OF EVENTS IN FORMATION OF PLAQUE

• Pellicle Formation:

It is a glycoprotein derived from salivary constituents which adsorbs rapidly onto newly cleaned tooth surfaces. It is the first step in plaque formation. Biochemical constituents of pellicle include albumin, lysozyme, amylase, immunoglobulin A, proline rich proteins and mucins1. Bacterial surface molecules interact with components of the pellicle, thus allowing bacteria to attach or adhere to the pellicle-coated tooth surface with the help of hair like structures called fimbriae.

• Primary colonization:

Pellicle–coated tooth surface is colonized by the Gram-positive ‘primary colonizers’ like Streptococcus mutans, Streptococcus sanguis and Actinomyces, which are mostly aerobic or facultative. The act of bacteria attaching to pellicle stimulates them to form an extra cellular slime layer. This helps them to stay anchored to the surface and also provides protection. This plaque biofilm grows rapidly through cell division of attached bacteria.

• Secondary colonization:

The plaque increases by:

1. Multiplication of primary colonizers                                                                                                                                                                                       
2. Primary colonizers produce substances that stimulate other free floating bacteria to join them, to form micro colonies. Attachment and multiplication of new bacterial species, or ‘secondary colonizers’, that are mostly Gram negative, like Fusobacterium nucleatum, Prevotella intermedia and Capnocytophaga species helps in growth of plaque.

3. Cell to cell communication: Dental plaque being a biofilm, the plaque cells communicate with each other in different ways like gene expression, cell to cell signaling (quorum sensing) and antibiotic resistance. This helps them to adapt and survive various environmental stresses. Specific bacteria in plaque biofilm can work together and impair the host.

• Tertiary colonization:

After about a week of plaque accumulation, few more species are seen in the plaque composition. They are called ‘tertiary colonizers’, and include Gram- negative species like Porphyromonus gingivalis,Campylobacter rectus, Eikenella corrodens, Actinobacillus actinomycetemcomitans and the oral spirochetes(Treponema species). As the plaque matures from primary to tertiary colonizers, the microbial ecology shifts from aerobic to anaerobic environment; favoring growth of anaerobic species. This mature plaque biofilm causes inflammation of gingival margins deepening the gingival sulcus. Thus the biofilm extends into subgingival region and grows in a well-protected area, forming the mature subgingival plaque.

PHASES OF PLAQUE FORMATION:

DISEASE PROCESS ASSOCIATED WITH PLAQUE

STATE OF HOMEOSTASIS:

The community of the matured plaque is diverse with many species being detected at different sites. The species composition is characterized by a degree of stability among the component species, even though minor environmental stresses are present. This stability or balance is termed as “microbial homeostasis”4. This is achieved by synergistic and antagonistic interactions between micro organisms.

DISTURBANCES IN HOMEOSTASIS:

Host defense and dietary compositions are of prime significance in maintaining homeostasis. Changes in critical parameters maintaining ecological stability may disrupt the homeostasis, a clinical manifestation of which may be seen as disease. Dietary factors such as frequent consumption of fermentable carbohydrates or inadequate maintenance of oral hygiene lead to pH changes, changing the microbial flora towards more pathogenic organisms, with loss of homeostasis.

CO-RELATION OF MICRO ORGANISMS WITH DISEASE:

Increase in pathogenic organisms and their colonies start causing deleterious effects on surrounding normal tissues of tooth or gingiva. There are multiple schools of thought describing the pathogenesis of disease, namely:

• SPECIFIC PLAQUE HYPOTHESIS:

Out of the many bacteria found in plaque, disease is associated with only a very limited group of organisms. Eg: Streptococci mutans and caries

• NON-SPECIFIC PLAQUE HYPOTHESIS:

Disease is due to the collective action of all the micro-organisms in plaque. Some organisms may have an active role in the disease process while others may have a neutral or protective influence

• ECOLOGICAL PLAQUE HYPOTHESIS:

Disease is due to change in local environmental condition which disrupts the natural balance between plaque and host leading to enrichment of organisms that can cause disease.

Plaque and Dental Caries:

• As plaque mass increases, saliva is less able to penetrate plaque and protect enamel; causing breakdown in plaque homeostasis.
• Frequent intake of dietary carbohydrates causes plaque pH to fall which favors the acidogenic and aciduric bacteria like Streptococci mutans and Lactobacilli to produce more acid which eventually demineralizes enamel resulting in caries.

Plaque and periodontitis:

• Accumulation of plaque around the gingival margin causes an inflammatory response to microbial challenge, resulting in increased gingival crevicular fluid (GCF) secretion and a small rise in local pH. This results in inflammation of gingiva, or gingivitis.
• Role of GCF: GCF not only delivers components of host defence, but also provides continuous supply of proteins, glycoproteins and co-factors that can act as novel nutrients for bacteria especially asacchyrolytic and obligatory anaerobes.
• The composition of plaque microflora shifts from aerobic to obligatory anaerobic; from Streptococci dominated microflora to one with higher levels of Actinomyces, Capnocytophaga, Fusobacterium and Prevotella species.
• As gingivitis progresses to periodontitis, more diverse microflora like Actinobacillus, Campylobacter, Selenomonas, Treponema, Wolinella can be seen.
• Direct activity of subgingival microflora and release of lysososmal enzymes and cytokines result in tissue damage.

PREVENTION OF DISEASE

For prevention of any diseases related to plaque, like caries or periodontitis, the conventional approach of meticulous cleaning by tooth brushing, flossing is necessary.

Prevention of dental caries:

• Avoidance of food or drinks containing fermentable sugars frequently between main meals.
• Fluoride application: fluorides inhibit the rapid fall in pH, maintaining microbial homeostasis.
• Remineralizing agents: help to restore minor areas of demineralization.
• Antimicrobial agent like chlorhexidine can be used as adjunct to mechanical cleaning for plaque control.
• Stimulation of salivary flow after main meals: As saliva is significant in clearing the fermentable sugars and also provides buffering action, stimulation of salivary flow can help in preventing caries. It can be done by use of sorbitol or xylitol containing chewing gums which are not only noncariogenic but also can promote remineralization by increasing salivary flow.

Prevention of periodontal disease4:

• Most conventional method is removal of subgingival plaque by meticulous cleaning.
• Use of antimicrobial and anti-inflammatory agents: Anti inflammatory agents may break tissue destruction and reduce flow of GCF. Triclosan and zinc citrate in combination can show greatest activity against periopathogens.
• Use of oxygenating and redox agents: As in disease the redox potential of pocket is reduced; to raise it use of redox dyes like methylene blue is proposed. This treatment significantly reduces GCF flow and proportion of obligate anaerobes.

CONCLUSION

Dental plaque is a structurally and functionally organized biofilm. It forms in an orderly manner and has a diverse microbial composition, which in ecological equilibrium is beneficial to the host. Dynamic balance between microbial interactions allows plaque to remain relatively stable despite minor disturbances. Any shift in the balance of micro flora disrupts the balance, predisposing the sites to disease. Plaque control goes a long way in prevention of disease and maintenance of oral health.

REFERENCES:

• Dr. Susan Kinder Haake, Microbiology of Dental Plaque; http://www.dent.ucla.edu/pic/members/microbio/mdphome.html
• microbe wiki
• Nield-Gehrig JS and Willmann DE. Foundations of Periodontics for the Dental Hygienist. Philadelphia: Lippincott Williams & Wilkins 2003:67-73.
• Marsh P.D., Microbial ecology of dental plaque and its significance in health and disease, Adv Dent Res 8(2): 263-271, July 1994.
• Marsh P.D., Dental plaque as a biofilm and a microbial community- implications for health and disease, BMC Oral Health 2006, 6(suppl1):S14