Dental plaque

From Wikipedia, the free encyclopedia
Jump to: navigation, search

Dental plaque is a biofilm or mass of bacteria that grows on surfaces within the mouth. It appears as a white/pale yellow "slime layer," that is commonly found in between the teeth and along the cervical margins.[1] Dental plaque is also known as microbial plaque, oral biofilm, dental biofilm, dental plaque biofilm or bacterial plaque biofilm.[1] While plaque is commonly associated with oral diseases such as caries and periodontal diseases (gum diseases), its formation is a normal process that can't be prevented. Its progression and build up is what leads to oral problems, hence why it is important to disrupt the mass of bacteria and remove it daily.[2] Plaque control and removal is achieved with correct tooth brushing and use of interdental aids (such as dental floss, interdental brush, etc.[1]

Removal of dental biofilm is important as it may become acidic causing demineralisation of the teeth also known as caries, or harden into calculus (dental) (also known as tartar).[3] Calculus cannot be removed through toothbrushing or use interdental aids and can only be removed through professional cleaning.[4] Therefore, removal of the dental biofilm will prevent the development of caries and/or gum diseases.[2]

Dental plaque can give rise to dental caries (tooth decay)—the localised destruction of the tissues of the tooth by acid produced from the bacterial degradation of fermentable sugar and periodontal problems such as gingivitis and periodontitis.[4]

Plaque formation[edit]

Dental plaque is a biofilm that attaches to tooth surfaces, restorations and prosthetic appliances (including dentures, bridge (dentistry), etc. Understanding the formation, composition and characteristics of plaque helps in its control.[5]

To put it simply, the three major phases of plaque development includes:

  1. Attachment of bacteria to a solid surface
  2. Formation of micro-colonies (microscopic communities of bacteria) on the surface
  3. Formation of mature, subgingival plaque biofilms [5]

The following provides a more detailed (six step) explanation of biofilm formation:

1. Association[edit]

  • Bacteria associates with the acquired dental pellicle. This is the initial stage of formation where a pellicle is formed from glycoproteins found in the saliva. Normally this pellicle acts as a protective layer for the tooth, however bacteria can attach to this pellicle. This pellicle formation provides the surface where bacteria can attach.

2. Adhesion[edit]

  • Within hours, bacteria loosely binds to the pellicle.

3. Proliferation[edit]

  • Bacteria spreads throughout the mouth and begins to multiply.

4. Microcolonies[edit]

  • Microcolonies are formed. Streptococci secrete protective layer (slime layer).

5. Biofilm formation[edit]

  • Microcolonies form complex groups with metabolic advantages.

6. Growth “Maturation”[edit]

  • The biofilm develops a primitive circulatory system.[6]

Components of plaque[edit]

In the oral cavity, there are different types of bacteria that normally present in the mouth. These bacteria including, leukocytes, neutrophils, macrophages, and lymphocytes are part of the normal oral cavity and contribute to the individual's health. Other oral cavity bacteria associated with periodontal health include Streptococcus it is, Actinomyces species and Streptococcus oralis and can be found supragingivally (above the gum).

The microorganisms that form the biofilm are mainly Streptococcus mutans and anaerobes, with the composition varying by location in the mouth. Examples of such anaerobes include fusobacterium and actinobacteria.[1] These microorganisms present in dental plaque are all naturally present in the oral cavity, and are normally harmless. However, failure to remove plaque by regular tooth brushing means that they are allowed to build up in a thick layer and cause dental disease. Those microorganisms nearest the tooth surface ferment dietary sucrose; it is in this state that they start to produce acids.

  • Acids released from dental plaque lead to demineralization of the adjacent tooth surface, and consequently to dental caries. Saliva is also unable to penetrate the build-up of plaque and thus cannot act to neutralize the acid produced by the bacteria and remineralize the tooth surface.
  • They also cause irritation of the gums around the teeth that could lead to gingivitis, periodontal disease and tooth loss.
  • Plaque build up can also become mineralized and form calculus (tartar).
    Calculus (tartar)

The extracellular matrix contains proteins, long chain polysaccharides and lipids.

As previously mentioned there are about 1,000 out of the 25,000 species of bacteria that are involved with the formation of dental biofilm. Due to this fairly large number there is fierce competition among the bacteria present on dental biofilm for nutrients present in the mouth. Only about fifty percent of the 1,000 species have been cultured for study.[7] Scientists at the Forsyth Institute in Cambridge, Massachusetts have begun the Human Oral Microbiome Project to identify bacteria and study the complex ecosystems of the mouth. On their website, one can find information about the identified organisms as well as the method being utilized to identify the organisms.

The microorganisms in the oral cavity live with one another in commensal or mutualistic symbiotic relationships.[8] Typically, anaerobic bacteria would succumb to high levels of oxygen, but with the redox reactions discussed in the previous section they are able to survive. This commensal relationship allows a mixture of aerobic and anaerobic bacteria to live in the same area. The formation begins by the adsorption of early colonizers onto an acquired pellicle through chemical processes.[9] An acquired pellicle is a layer of saliva that is composed of mainly glycoproteins and forms shortly after cleaning of the teeth or exposure of new teeth.[9] These bound early colonizers manipulate the environment for the immediate benefit of other bacteria. Once the environment has been manipulated other bacterial colonizers are able to co-adhere to the early colonizers. This is done repeatedly resulting in layers of bacteria. Once new bacterial cells co-adhere to one another they gain the ability to communicate to one another. They are able to communicate to one another through a biochemical process called quorum sensing.[7] Quorum sensing virtually allows all the bacteria to benefit from one another. This ability can allow a bacterium to feel the presence of other bacteria around it. Due to this communication, bacteria have the ability to change their genotype (and thus their phenotype) as a result of population concentration and/or environmental changes to remain as competent competitors.[10] These relationships tend to exhibit homeostasis until there is some type of disruption in the ecosystem.

The most common reasons for ecosystem disruption are the ecological factors discussed in the environment section. The bacteria that exhibits the most fit plasticity for the change in environment dominates the given environment. Often, this could lead to opportunistic pathogens that lead to dental caries and periodontal disease. Pathogens that have the potential to cause dental caries flourish in acidic environments. Pathogenic bacteria that have the potential to cause periodontal disease flourish in a slightly alkaline environment.[11]


The ecological factors provided by the environment of the mouth cavity are directly proportional to the species richness and species biodiversity of the microorganisms that reside on the teeth.[8] The main ecological factors are pH, saliva, temperature and redox reactions.[8][12] The majority of microbial organisms prefer neutral pH levels (pH 7). Saliva acts as a buffer, maintaining the pH in the mouth between 6.75 and 7.25.[8] In addition to acting as a buffer, saliva is also a main source of nutrients for the thousands of bacteria (note: gingival crevicular fluid is also a nutrient source but a smaller one ). A two degree (°C) change has been shown to drastically shift the dominant species in the plaque.[12] The normal temperature of the mouth ranges between 35–36 °C (Marsh). Redox reactions are carried out by aerobic bacteria. This keeps the oxygen levels in the mouth at a semi-stable homeostatic condition. This allows other bacteria to survive, which will be discussed in the next section.[12]

Consequence of plaque build up[edit]


Top: typical presentation of gingivitis Bottom: healthy gingiva

Gingivitis is a common result of plaque build up around the gingival tissues. The bacteria found in the biofilm elicit a host response resulting in localized inflammation of the tissue.[13] This is characterized by the cardinal signs of inflammation including a red, puffy appearance of the gums and bleeding due to brushing or flossing.[14] Gingivitis due to plaque can be reversible by removal of the cause, plaque. However if left for an extended period the inflammation may begin to affect the supporting tissues, this progression is referred to as Periodontal Disease or Periodontitis.[15]


Loss of bone due to periodontal disease

Periodontitis is an infection of the gums which leads to bone destruction around the teeth in the jaw. Periodontitis occurs after gingivitis has been established, but not all individuals who have gingivitis will get periodontitis.[16][17] Plaque accumulation is vital in the progression of periodontitis as the bacteria in plaque release enzymes which attack the bone and cause is to break down, and at the same time the osteoclasts in the bone breakdown the bone as a way to prevent further infection. This can be treated with strict oral hygiene such as tooth brushing and cleaning in between the teeth and as well as surgical debridement completed by a dental professional.[18]


Representation of the progression of Dental Caries

Dental caries is an infectious disease caused primarily by Streptococcus mutans, characterized by acid demineralization of the enamel, which can progress to further breakdown of the more organic, inner dental tissue.[1] Everybody is susceptible to caries but the probability of development depends on the patient’s individual disease indicators, risk factors and preventive factors. Factors that are considered high risk for developing carious lesions include; exposure to fluoride, time, length and frequency of sugar consumption, quality of tooth cleaning, fluctuations in salivary flow rates and composition, behaviour of the individual, socio economic status of the individual and finally quality and composition of biofilms.[1]

Detection of plaque build up[edit]

Plaque detection is usually detected clinically by plaque disclosing agents. Disclosing agents contain dye which turns bright red to indicate plaque buildup.

There are two main methods of detecting dental plaque in the oral cavity; through the application of a disclosing gel/tablet and/or visually through observation. It is important for an individual to be aware of what to look for when doing a self assessment for dental plaque. It is important to be aware that everyone has dental plaque, however there are varying levels of severity and consequences of not removing the dental plaque biolfilm.

Plaque Disclosing gel or tablets[edit]

Plaque disclosing are also known as disclosants, it makes plaque clinically visible. Clean surfaces of the teeth do not absorb the disclosant, only rough surfaces. Plaque disclosing gels can be either completed at home or in the dental clinic. Before using these at home or in the dental clinic check with your general practitioners for any allergies for Iodine, food colouring or any other ingredients that may be present in these products. These gels provide a visual aid in assessing plaque biolfim presence and can also show the maturity of the dental plaque.

Disclosing tablets[edit]

Disclosing tablets are similar to that of disclosing gels. However they are placed in the mouth and chewed on for approximately one minute. The remaining tablet or saliva is then spit out. Disclosing gels will show the presence of the plaque, however will often not show the level of maturity of the plaque. Disclosing tablets are often prescribed or given to patients with orthodontic appliances for use before and after toothbrushing to ensure optimal cleaning. These are also helpful educational tools for young children or patients that are struggling to remove dental plaque in certain areas.

Disclosing gels and tablets are useful for individuals of all ages in ensuring efficient dental plaque removal.

Visual or tactile detection dental plaque[edit]

Dental biofilm forms on the tooth only minutes after brushing. It can be difficult to visualise dental plaque on the hard tissue surfaces, however a rough surface can be felt after eating or before toothbrushing if there is a thick deposit of dental plaque. It is often felt as a thick, furlike deposit that may present as a yellow, tan or brown stain. They are commonly found on teeth on dental appliances such as orthodontic brackets, and the tongue. The most common way dental plaque is assess is through dental assessment in the dental clinic where dental instruments are able to scrape up some plaque.

The most common areas where patients find plaque is often in between the teeth or along the cervical margins as shown in the image below.

See also[edit]


  1. ^ a b c d e f Darby M L, Walsh M M. Dental Hygiene Theory and Practice. 2010.
  2. ^ a b Verkaik M, Busscher H, Jager D, Slomp A, Abbas F, van der Mei H. Efficacy of natural antimicrobials in toothpaste formulations against oral biofilms in vitro. Journal of Dentistry. 2011;39(3):218-224.
  3. ^ Summitt J, R. J., Hilton T, Schwartz R. (2006). Fundamentals of Operative Dentistry. 4350 Chandler Drive, Hanover Park, Illinois.
  4. ^ a b Wolf H and Hassell T (2006). Color Atlas of Dental Hygiene Thieme New York, 333 Seventh Avenue, New York, USA.
  5. ^ a b Chetrus V and Ion I.R (2013). "Dental Plaque - Classification, Formation, and Identification." Int. J. Med. Detistry 3: 139-143.
  6. ^ Nield-Gehrig J and Willmann D (2011). Foundations of Periodontics for the Dental Hygienist Wolters Kluwer Health | Lippincott Williams & Wilkins.
  7. ^ a b ten Cate, Jacob M. (2006). "Biofilms, a new approach to the microbiology of dental plaque". Odontology (Springer Publishing) 94 (1): 1–9. doi:10.1007/s10266-006-0063-3. Retrieved 2012-08-22. 
  8. ^ a b c d Marsh, P.D. (February 2003). "Are dental diseases examples of ecological catastrophes?". Microbiology (Society for General Microbiology) 143 (2): 279–294. doi:10.1099/mic.0.26082-0. Retrieved 2012-08-22. 
  9. ^ a b Kreth, Jens; Merritt, J.; Qi, F. (August 2009). "Bacterial and Host Interactions of Oral Streptococci". DNA and Cell Biology (Mary Ann Liebert, Inc.) 28 (8): 397–403. doi:10.1089/dna.2009.0868. Retrieved 2012-08-22. 
  10. ^ Thomas, J.G.; Nakaishi, L.A. (2006). "Managing the Complexity of a dynamic biofilm". Journal of the American Dental Association (American Dental Association) 137 (suppl. 3): 10S–15S. Retrieved 2012-08-22. 
  11. ^ Garcia, F.; Hicks, M.J. (May 2008). "Maintaining the Integrity of the Enamel Surface: The role of dental biofilm, saliva, and preventative agents in the enamel demineralization and remineralization". Journal of the American Dental Association (American Dental Association) 139 (suppl. 2): 25S–34S. Retrieved 2012-08-22. 
  12. ^ a b c Marsh, P.D.; Devine, D.A. (February 2011). "How is the development of dental biofilms influenced by the host?". Journal of Clinical Periodontology (John Wiley & Sons) 38 (s11): 28–35. doi:10.1111/j.1600-051X.2010.01673.x. Retrieved 2012-08-22. 
  13. ^ The American Academy of Periodontology. Proceedings of the World Workshop in Clinical Periodontics. Chicago:The American Academy of Periodontology; 1989:I/23-I/24.
  14. ^ Parakrama Chandrasoma, Clive R. Taylor (c. 2005). "Part A. General Pathology, Section II. The Host Response to Injury, Chapter 3. The Acute Inflammatory Response, sub-section Cardinal Clinical Signs". Concise Pathology (3rd edition (Computer file) ed.). New York, N.Y.: McGraw-Hill. ISBN 0-8385-1499-5. OCLC 150148447. Retrieved 2008-11-05. 
  15. ^ Noble SL. Clinical Textbook of Dental Hygiene and Therapy, 2nd ed. West Sussex, Wiley-Blackwell; 2012. p. 96-97.
  16. ^ Noble SL. Clinical Textbook of Dental Hygiene and Therapy, 2nd ed. West Sussex, Wiley-Blackwell; 2012. p. 111.
  17. ^ Rateitschak KH, Rateitschak EM, Wolf HF, Hassell TM. Color Atlas of Periodontology, New York, Thieme Inc; 1985. p.55
  18. ^ Tonetti M S, Eickholz P, Loos B G, Papapanou P, van der Velden U, Armitage G, Bouchard P, Deinzer R, Dietrich T, Hughes F, Kocher T, Lang N P, Lopez R, Needleman I, Newton T, Nibali L, Pretzl B, Ramseier C, Sanz-Sanchez I, Schlagenhauf U, Suvan J E, Fabrikant E, Fundak A. Principles in Prevention of Periodontal Diseases.. Journal of Clinical Periodontology 2015,

External links[edit]