Dental plaque

Dental plaque is a biofilm of microorganisms (mostly bacteria, but also fungi) that grows on surfaces
within the mouth. It is a sticky colorless deposit at first, but when it forms tartar, it is often brown or pale
yellow. It is commonly found between the teeth, on the front of teeth, behind teeth, on chewing surfaces,
along the gumline (supragingival), or below the gumline cervical margins (subgingival).[1] Dental plaque is
also known as microbial plaque, oral biofilm, dental biofilm, dental plaque biofilm or bacterial plaque
biofilm. Bacterial plaque is one of the major causes for dental decay and gum disease.[1]

Progression and build-up of dental plaque can give rise to 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;[2] hence it is important to disrupt the mass of bacteria and
remove it.[3] Plaque control and removal can be achieved with correct daily or twice-daily tooth brushing
and use of interdental aids such as dental floss and interdental brushes.[1]

Oral hygiene is important as dental biofilms may become acidic causing demineralization of the teeth (also
known as dental caries) or harden into dental calculus (also known as tartar).[4] Calculus cannot be
removed through tooth brushing or with interdental aids, but only through professional cleaning.[2]

Contents
Plaque formation
Components of plaque
Bacteria
Dental plaque as a biofilm
Early colonisers
Late colonisers
Supragingival biofilm
Subgingival biofilm
Environment
Consequences of plaque build-up
Gingivitis
Periodontitis
Diseases linked to periodontitis
Caries
Detection of plaque build-up
Plaque disclosing gel
Disclosing tablets
Visual or tactile detection
Plaque in dogs and cats
See also
References
External links

Plaque formation
Dental plaque is a biofilm that attaches to tooth surfaces, restorations and prosthetic appliances (including
dentures and bridges) if left undisturbed. Understanding the formation, composition and characteristics of
plaque helps in its control.[5] 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.[6] Bacteria then attach
to the pellicle layer, form micro-colonies, and mature on the tooth, which can result in oral diseases. The
following table provides a more detailed (six-step) explanation of biofilm formation:

Simple description of the different steps involved in plaque formation

Components of plaque
Different types of bacteria are normally present in the mouth. These bacteria, as well as leukocytes,
neutrophils, macrophages, and lymphocytes, are part of the normal oral cavity and contribute to the
individual's health.[1] Approximately 80–90% of the weight of plaque is water. While 70% of the dry
weight is bacteria, the remaining 30% consists of polysaccharides and glycoproteins.[7]

Bacteria

The bulk of the microorganisms that form the biofilm are Streptococcus mutans and other anaerobes,
though the precise composition varies by location in the mouth. Examples of such anaerobes include
fusobacterium and actinobacteria.[1] S. mutans and other anaerobes are the initial colonisers of the tooth
surface, and play a major role in the establishment of the early biofilm community.[8] Streptococcus mutans
uses the enzyme glucansucrase to convert sucrose into a sticky, extracellular, dextran-based polysaccharide
that allows the bacteria to cohere, forming plaque. (Sucrose is the only sugar that bacteria can use to form
this sticky polysaccharide).[9] These microorganisms all occur naturally in the oral cavity and are normally
harmless. However, failure to remove plaque by regular tooth-brushing allows them to proliferate
unchecked and thereby build up in a thick layer, which can by virtue of their ordinary metabolism cause
any of various dental diseases for the host. Those microorganisms nearest the tooth surface typically obtain
energy by fermenting dietary sucrose; during fermentation they begin to produce acids.

The bacterial equilibrium position varies at different stages of formation. Below is a summary of the
bacteria that may be present during the phases of plaque maturation:

Early biofilm: primarily Gram-positive cocci

 Older biofilm (3–4 days): increased numbers of filaments and fusiforms
4–9 days undisturbed: more complex flora with rods, filamentous forms
7–14 days: Vibrio species, spirochetes, more Gram-negative organisms[10]

Dental plaque as a biofilm

Dental plaque is considered a biofilm adhered to the tooth surface. It is a meticulously formed microbial
community, that is organised to a particular structure and function.[11] Plaque is rich in species, given the
fact that about 1000 different bacterial species have been recognised using modern techniques.[12]

A clean tooth surface would immediately be colonised by salivary pellicles, which acts as an adhesive. This
allows the first bacteria (early colonisers) to attach to the tooth, then colonise and grow. After some growth
of early colonisers, the biofilm becomes more compliant to other species of bacteria, known as late
colonisers.[12]

Early colonisers
[12]

mainly Streptococcus species (60–90%)

Eikenella spp.
Haemophilus spp.
Prevotella spp.
Propionibacterium spp.
Capnocytophaga spp.
Veillonella spp.

Late colonisers
[12]

Aggregatibacter actinomycetemcomitans
Prevotella intermedia
Eubacterium spp.
Treponema spp.
Porphyromonas gingivalis

Fusobacterium nucleatum is found between the early and late colonisers, linking them together.

Some salivary components are crucial for plaques ecosystem, such as salivary alpha-amylase which plays a
role in binding and adhesion.[13] Proline-rich proteins (PRP) and statherins are also involved in the
formation of plaque.[12]

Supragingival biofilm
Supragingival biofilm is dental plaque that forms above the gums, and is the first kind of plaque to form
after the brushing of the teeth. It commonly forms in between the teeth, in the pits and grooves of the teeth
and along the gums. It is made up of mostly aerobic bacteria, meaning these bacteria need oxygen to
survive. If plaque remains on the tooth for a longer period of time, anaerobic bacteria begin to grow in this
plaque.[5]

Subgingival biofilm

Subgingival biofilm is plaque that is located under the gums. It

occurs after the formation of the supragingival biofilm by a
downward growth of the bacteria from above the gums to below.
This plaque is mostly made up of anaerobic bacteria, meaning that
these bacteria will only survive if there is no oxygen. As this plaque
attaches in a pocket under the gums, they are not exposed to
oxygen in the mouth and will therefore thrive if not removed.[10]
Heavy plaque
The extracellular matrix contains proteins, long-chain
polysaccharides and lipids.

The most common reasons for ecosystem disruption are the ecological factors discussed in the environment
section. The bacteria that exhibit the most fit plasticity for the change in environment dominate the given
environment. Often, this leads to opportunistic pathogens which may cause dental caries and periodontal
disease. Pathogenic bacteria that have the potential to cause dental caries flourish in acidic environments;
those that have the potential to cause periodontal disease flourish in a slightly alkaline environment.[14]

Antibodies to the oral pathogens Campylobacter rectus, Veillonella parvula, Prevotella melaninogenica
were associated with hypertension.[15]

Environment
Unlike other parts of the body, tooth surfaces are uniquely hard and non shedding. Therefore, the warm and
moist environment of the mouth and the presence of teeth, makes a good environment for growth and
development of dental plaque.[12] The main ecological factors that contribute to plaque formation are pH,
saliva, temperature and redox reactions.[16][17] The normal pH range of saliva is between 6 and 7 and
plaque biofilm is known to flourish in a pH between 6.7 and 8.3.[18][19] This indicates that the natural
environment of the mouth provided by saliva is ideal for the growth of bacteria in the dental plaque. Saliva
acts as a buffer, which helps to maintain the pH in the mouth between 6 and 7.[16] In addition to acting as a
buffer, saliva and gingival crevicular fluid contain primary nutrients including amino acids, proteins and
glycoproteins. This feeds the bacteria involved in plaque formation. The host diet plays only a minor role in
providing nutrients for the resident microflora.[20] The normal temperature of the mouth ranges between 35
and 36 °C, and a two-degree (°C) change has been shown to drastically shift the dominant species in the
plaque.[17] Redox reactions are carried out by aerobic bacteria. This keeps the oxygen levels in the mouth
at a semi-stable homeostatic condition, which allows the bacteria to survive.[17]

Consequences of plaque build-up

Gingivitis
Gingivitis is an inflammatory lesion, mediated by host-parasite
interactions that remains localised to the gingival tissue, it 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.[21] This is characterized by the
cardinal signs of inflammation including a red, puffy appearance of
the gums and bleeding due to brushing or flossing.[22]
Gingivitis
due to plaque can be reversible by removal of the plaque. However,
if left for an extended period of time, the inflammation may begin
to affect the supporting tissues, in a progression referred to as
periodontitis.[23]: 9 6–97  The gingivitis response is a protective
Top: typical presentation of gingivitis.
mechanism, averting periodontitis in many cases.
Bottom: healthy gingiva.

Periodontitis

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.[23]: 1 11 [24] Plaque accumulation is
vital in the progression of periodontitis as the bacteria in plaque Loss of bone due to periodontal
release enzymes which attack the bone and cause it to break down, disease
and at the same time osteoclasts in the bone break down 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 as well as surgical debridement
completed by a dental professional.[25]

Diseases linked to periodontitis

Accumulated bacteria, due to the onset of periodontitis from dental plaque, may gain access to distant sites
in the body through the circulatory and respiratory system, potentially contributing to various systematic
diseases and conditions. Due to the infectious nature of bacteria hosted within the oral cavity, bacteria
produced cavity can spread within the system of the human body and causes adverse health conditions.[26]
Bacteria access comes from the ulcerated epithelium of the periodontal pocket that results from
accumulation of infection within the gingiva. Conditions and diseases can include:

Atheromas[27]

Cardiovascular disease[28]
Respiratory disease[29]
Diabetes mellitus[30]

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 (dentin).[1] The bacterial community would mainly consist of acidogenic and acid-tolerating species
(e.g. Mutans streptococci and lactobacilli), while other species with relevant characteristics may also be
involved.[31] 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 on the teeth include:

Low fluoride exposure

Time, length, and frequency of sugar consumption
Quality of tooth cleaning
Fluctuations in salivary flow rates and composition
Behavior of the individual
Quality and composition of biofilms[1]

Organic acids released from dental plaque lead to demineralization of the adjacent
Representation of
the progression of
tooth surface, and consequently to dental caries. Saliva is also unable to penetrate the
dental caries build-up of plaque and thus cannot act to neutralize the acid produced by the bacteria
and remineralize the tooth surface.

Detection of plaque build-up

There are two main methods of detecting dental plaque in the oral cavity: through the application of a
disclosing gel or tablet, and/or visually through observation. Plaque detection is usually detected clinically
by plaque disclosing agents. Disclosing agents contain dye which turns bright red to indicate plaque build-
up.[1]

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, the severity of the build-up
and the consequences of not removing the plaque can vary.[1]

Plaque disclosing gel

Plaque disclosing products, also known as disclosants, make 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 to iodine, food colouring or any other ingredients
that may be present in these products. These gels provide a visual
aid in assessing plaque biofilm presence and can also show the
maturity of the dental plaque.

Disclosing tablets Plaque disclosing gel: before (top)

and after (bottom)
Disclosing tablets are similar to that of disclosing gels, except that
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,
but 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 tooth brushing to ensure optimal cleaning.
These are also helpful educational tools for young children or patients who 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 biofilm begins to form on the tooth only minutes after

brushing. It can be difficult to see dental plaque on the hard tissue
surfaces, however it can be felt as a rough surface. It is often felt as
a thick, fur-like deposit that may present as a yellow, tan or brown
stain. These deposits are commonly found on teeth or dental
appliances such as orthodontic brackets. The most common way
dental plaque is assessed is through dental assessment in the dental
clinic where dental instruments are able to scrape up some plaque. Disclosing dental plaque with
The most common areas where patients find plaque are between disclosing tablets
the teeth and along the cervical margins.

Plaque in dogs and cats

Dental plaque is also extremely common in domestic animals such as dogs and cats. However, the bacteria
associated with canine and feline plaque appear to be different from those of humans.[32][33] If untreated it
can lead to more severe gum disease such as periodontitis; hence veterinarians often recommend oral
healthcare products for affected pets.

See also
Flossing
Gingiva
Dental disease
Oral hygiene
Oral microbiology

References
1. Darby ML, Walsh MM (2010). Dental Hygiene Theory and Practice.
2. Wolf H, Hassell T (2006). Color Atlas of Dental Hygiene. New York: Thieme.
3. Verkaik MJ, Busscher HJ, Jager D, Slomp AM, Abbas F, van der Mei HC (March 2011).
"Efficacy of natural antimicrobials in toothpaste formulations against oral biofilms in vitro" (htt
ps://pure.rug.nl/ws/files/6760238/Efficacyofnaturalantimicrobialsinto.pdf) (PDF). Journal of
Dentistry. 39 (3): 218–24. doi:10.1016/j.jdent.2010.12.007 (https://doi.org/10.1016%2Fj.jden
t.2010.12.007). hdl:11370/da862a1c-8bdc-4d47-b6c4-3b43e87309c6 (https://hdl.handle.net/
11370%2Fda862a1c-8bdc-4d47-b6c4-3b43e87309c6). PMID 21195122 (https://pubmed.nc
bi.nlm.nih.gov/21195122).
4. Summitt JB, Robbins JW, Hilton TJ, Schwartz RS (2006). Fundamentals of Operative
Dentistry: A Contemporary Approach. ISBN 978-0-86715-452-8.
5. Chetrus V, Ion IR (2013). "Dental Plaque – Classification, Formation, and Identification".
International Journal of Medical Dentistry. 17 (2): 139–143.
6. Kreth J, Merritt J, Qi F (August 2009). "Bacterial and host interactions of oral streptococci" (ht
tps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2903342). DNA and Cell Biology. 28 (8): 397–
403. doi:10.1089/dna.2009.0868 (https://doi.org/10.1089%2Fdna.2009.0868).
PMC 2903342 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2903342). PMID 19435424
(https://pubmed.ncbi.nlm.nih.gov/19435424).
 7. Marsh PD, Bradshaw DJ (September 1995). "Dental plaque as a biofilm". Journal of
Industrial Microbiology. 15 (3): 169–75. doi:10.1007/BF01569822 (https://doi.org/10.1007%2
FBF01569822). PMID 8519474 (https://pubmed.ncbi.nlm.nih.gov/8519474).
S2CID 22742494 (https://api.semanticscholar.org/CorpusID:22742494).
8. Kolenbrander PE (2000). "Oral microbial communities: biofilms, interactions, and genetic
systems". Annual Review of Microbiology. 54: 413–37. doi:10.1146/annurev.micro.54.1.413
(https://doi.org/10.1146%2Fannurev.micro.54.1.413). PMID 11018133 (https://pubmed.ncbi.n
lm.nih.gov/11018133).
9. Ryan KJ, Ray CG, eds. (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill.
ISBN 978-0-8385-8529-0.
10. Wilkins E. Clinical Practice of the Dental Hygienist. Philadelphia: Wolters Kluwer
Health/Lippincott Williams & Wilkins; 2009
11. Marsh PD (June 2006). "Dental plaque as a biofilm and a microbial community - implications
for health and disease" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2147593). BMC Oral
Health. 6 Suppl 1 (Suppl 1): S14. doi:10.1186/1472-6831-6-S1-S14 (https://doi.org/10.118
6%2F1472-6831-6-S1-S14). PMC 2147593 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC
2147593). PMID 16934115 (https://pubmed.ncbi.nlm.nih.gov/16934115).
12. ten Cate JM (September 2006). "Biofilms, a new approach to the microbiology of dental
plaque". Odontology. 94 (1): 1–9. doi:10.1007/s10266-006-0063-3 (https://doi.org/10.1007%
2Fs10266-006-0063-3). PMID 16998612 (https://pubmed.ncbi.nlm.nih.gov/16998612).
S2CID 24330907 (https://api.semanticscholar.org/CorpusID:24330907).
13. Scannapieco FA, Torres G, Levine MJ (1993). "Salivary alpha-amylase: role in dental plaque
and caries formation". Critical Reviews in Oral Biology and Medicine. 4 (3–4): 301–7.
CiteSeerX 10.1.1.542.3621 (https://citeseerx.ist.psu.edu/viewdoc/summary?doi=10.1.1.542.
3621). doi:10.1177/10454411930040030701 (https://doi.org/10.1177%2F104544119300400
30701). PMID 8373987 (https://pubmed.ncbi.nlm.nih.gov/8373987).
14. García-Godoy F, Hicks MJ (May 2008). "Maintaining the integrity of the enamel surface: the
role of dental biofilm, saliva and preventive agents in enamel demineralization and
remineralization". Journal of the American Dental Association. 139 (Suppl 2): 25S–34S.
doi:10.14219/jada.archive.2008.0352 (https://doi.org/10.14219%2Fjada.archive.2008.0352).
PMID 18460677 (https://pubmed.ncbi.nlm.nih.gov/18460677).
15. Pietropaoli, Davide; Del Pinto, Rita; Ferri, Claudio; Ortu, Eleonora; Monaco, Annalisa
(August 2019). "Definition of hypertension-associated oral pathogens in NHANES". Journal
of Periodontology. 90 (8): 866–876. doi:10.1002/JPER.19-0046 (https://doi.org/10.1002%2F
JPER.19-0046). ISSN 1943-3670 (https://www.worldcat.org/issn/1943-3670).
PMID 31090063 (https://pubmed.ncbi.nlm.nih.gov/31090063). S2CID 155089995 (https://ap
i.semanticscholar.org/CorpusID:155089995).
16. Marsh PD (February 2003). "Are dental diseases examples of ecological catastrophes?" (htt
p://mic.sgmjournals.org/content/149/2/279.long). Microbiology. 149 (Pt 2): 279–94.
doi:10.1099/mic.0.26082-0 (https://doi.org/10.1099%2Fmic.0.26082-0). PMID 12624191 (htt
ps://pubmed.ncbi.nlm.nih.gov/12624191).
17. Marsh PD, Devine DA (March 2011). "How is the development of dental biofilms influenced
by the host?" (https://doi.org/10.1111%2Fj.1600-051X.2010.01673.x). Journal of Clinical
Periodontology. 38 Suppl 11 (s11): 28–35. doi:10.1111/j.1600-051X.2010.01673.x (https://d
oi.org/10.1111%2Fj.1600-051X.2010.01673.x). PMID 21323701 (https://pubmed.ncbi.nlm.ni
h.gov/21323701).
18. Humphrey SP, Williamson RT (February 2001). "A review of saliva: normal composition,
flow, and function". The Journal of Prosthetic Dentistry. 85 (2): 162–9.
doi:10.1067/mpr.2001.113778 (https://doi.org/10.1067%2Fmpr.2001.113778).
PMID 11208206 (https://pubmed.ncbi.nlm.nih.gov/11208206).
19. McDermid AS, McKee AS, Marsh PD (May 1988). "Effect of environmental pH on enzyme
activity and growth of Bacteroides gingivalis W50" (https://www.ncbi.nlm.nih.gov/pmc/article
s/PMC259768). Infection and Immunity. 56 (5): 1096–100. doi:10.1128/iai.56.5.1096-
1100.1988 (https://doi.org/10.1128%2Fiai.56.5.1096-1100.1988). PMC 259768 (https://www.
ncbi.nlm.nih.gov/pmc/articles/PMC259768). PMID 3281900 (https://pubmed.ncbi.nlm.nih.go
v/3281900).
20. Marsh PD, Moter A, Devine DA (February 2011). "Dental plaque biofilms: communities,
conflict and control". Periodontology 2000. 55 (1): 16–35. doi:10.1111/j.1600-
0757.2009.00339.x (https://doi.org/10.1111%2Fj.1600-0757.2009.00339.x). PMID 21134226
(https://pubmed.ncbi.nlm.nih.gov/21134226).
21. Armitage GC (December 1999). "Development of a classification system for periodontal
diseases and conditions". Annals of Periodontology. 4 (1): 1–6.
doi:10.1902/annals.1999.4.1.1 (https://doi.org/10.1902%2Fannals.1999.4.1.1).
PMID 10863370 (https://pubmed.ncbi.nlm.nih.gov/10863370). S2CID 24243752 (https://api.s
emanticscholar.org/CorpusID:24243752).
22. Chandrasoma P, Taylor CR (c. 2005). "Part A. General Pathology, Section II. The Host
Response to Injury, Chapter 3. The Acute Inflammatory Response, sub-section Cardinal
Clinical Signs" (http://www.accessmedicine.com/content.aspx?aID=183351). Concise
Pathology (http://www.accessmedicine.com/resourceTOC.aspx?resourceID=7) (3rd edition
(Computer file) ed.). New York, N.Y.: McGraw-Hill. ISBN 978-0-8385-1499-3.
OCLC 150148447 (https://www.worldcat.org/oclc/150148447). Retrieved 2008-11-05.
23. Noble SL (2012). Clinical Textbook of Dental Hygiene and Therapy (2nd ed.). West Sussex:
Wiley-Blackwell. pp. 96–97.
24. Rateitschak KH, Rateitschak EM, Wolf HF, Hassell TM (1985). Color Atlas of
Periodontology. New York: Thieme Inc. p. 55.
25. Tonetti MS, Eickholz P, Loos BG, Papapanou P, van der Velden U, Armitage G, et al. (April
2015). "Principles in prevention of periodontal diseases: Consensus report of group 1 of the
11th European Workshop on Periodontology on effective prevention of periodontal and peri-
implant diseases" (https://doi.org/10.1111%2Fjcpe.12368). Journal of Clinical
Periodontology. 42 Suppl 16: S5–11. doi:10.1111/jcpe.12368 (https://doi.org/10.1111%2Fjc
pe.12368). PMID 25639948 (https://pubmed.ncbi.nlm.nih.gov/25639948).
26. Gulati M, Anand V, Jain N, Anand B, Bahuguna R, Govila V, Rastogi P (September 2013).
"Essentials of periodontal medicine in preventive medicine" (https://www.ncbi.nlm.nih.gov/p
mc/articles/PMC3793498). International Journal of Preventive Medicine. 4 (9): 988–94.
PMC 3793498 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3793498). PMID 24130938
(https://pubmed.ncbi.nlm.nih.gov/24130938).
27. Han YW (February 2015). "Fusobacterium nucleatum: a commensal-turned pathogen" (http
s://www.ncbi.nlm.nih.gov/pmc/articles/PMC4323942). Current Opinion in Microbiology. 23:
141–7. doi:10.1016/j.mib.2014.11.013 (https://doi.org/10.1016%2Fj.mib.2014.11.013).
PMC 4323942 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4323942). PMID 25576662
(https://pubmed.ncbi.nlm.nih.gov/25576662).
28. "Inflammation: The Relationship Between Oral and Systemic Health - CDEWorld" (https://ad
aa.cdeworld.com/courses/20776-Inflammation:The_Relationship_Between_Oral_and_Syst
emic_Health). adaa.cdeworld.com. Retrieved 2019-05-17.
29. Scannapieco FA (July 1999). "Role of oral bacteria in respiratory infection". Journal of
Periodontology. 70 (7): 793–802. doi:10.1902/jop.1999.70.7.793 (https://doi.org/10.1902%2F
jop.1999.70.7.793). PMID 10440642 (https://pubmed.ncbi.nlm.nih.gov/10440642).
30. Löe H (January 1993). "Periodontal disease. The sixth complication of diabetes mellitus".
Diabetes Care. 16 (1): 329–34. doi:10.2337/diacare.16.1.329 (https://doi.org/10.2337%2Fdia
care.16.1.329). PMID 8422804 (https://pubmed.ncbi.nlm.nih.gov/8422804). S2CID 7257038
(https://api.semanticscholar.org/CorpusID:7257038).
31. Marsh PD (June 2006). "Dental plaque as a biofilm and a microbial community - implications
for health and disease" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2147593). BMC Oral
Health. 6 Suppl 1: S14. doi:10.1186/1472-6831-6-S1-S14 (https://doi.org/10.1186%2F1472-
6831-6-S1-S14). PMC 2147593 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2147593).
PMID 16934115 (https://pubmed.ncbi.nlm.nih.gov/16934115).
32. Dewhirst FE, Klein EA, Bennett ML, Croft JM, Harris SJ, Marshall-Jones ZV (February
2015). "The feline oral microbiome: a provisional 16S rRNA gene based taxonomy with full-
length reference sequences" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4297541).
Veterinary Microbiology. 175 (2–4): 294–303. doi:10.1016/j.vetmic.2014.11.019 (https://doi.o
rg/10.1016%2Fj.vetmic.2014.11.019). PMC 4297541 (https://www.ncbi.nlm.nih.gov/pmc/artic
les/PMC4297541). PMID 25523504 (https://pubmed.ncbi.nlm.nih.gov/25523504).
33. Dewhirst FE, Klein EA, Thompson EC, Blanton JM, Chen T, Milella L, Buckley CM, Davis IJ,
Bennett ML, Marshall-Jones ZV (2012). "The canine oral microbiome" (https://www.ncbi.nlm.
nih.gov/pmc/articles/PMC3338629). PLOS ONE. 7 (4): e36067.
Bibcode:2012PLoSO...736067D (https://ui.adsabs.harvard.edu/abs/2012PLoSO...736067D).
doi:10.1371/journal.pone.0036067 (https://doi.org/10.1371%2Fjournal.pone.0036067).
PMC 3338629 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3338629). PMID 22558330
(https://pubmed.ncbi.nlm.nih.gov/22558330).

External links
A Biofilm Primer (http://www.personal.psu.edu/faculty/j/e/jel5/biofilms/primer.html) Archived
(https://web.archive.org/web/20180716194823/http://www.personal.psu.edu/faculty/j/e/jel5/bi
ofilms/primer.html) 2018-07-16 at the Wayback Machine

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