Bacterial Plaque and its Relationship to Dental Disease

Bacterial plaque is described as colonies of microorganisms rooted in a matrix and adhered to

various surfaces in the oral cavity. It is composed of 80% water and 20% solids (mainly calcium,

phosphorus, and macronutrients) (Clark, 2017). The matrix produced by the microorganisms is

made up of mostly proteins and polysaccharides and creates a protective barrier resistant to

antimicrobials and the human immune system. The surfaces affected include the tooth surface,

gingiva, calculus, prostheses and dental appliances potentially present in the mouth. It is dense

and can be removed with a toothbrush and floss or an alternative floss aid. Formation occurs by

bacteria attaching itself to the acquired pellicle on the tooth surface via physical and chemical

processes (Wilkins, 2017). The bacteria begin to organize and communicate via chemical

signals, and will multiply and mature and eventually form the aforementioned matrix. Bacteria

embedded in a matrix is much more tenacious and dangerous than free-floating bacteria

(Overman 2017). Plaque or biofilm left undisturbed can lead to serious inflammatory dental

diseases associated with the hard and soft tissues of the mouth such as caries, gingivitis, and

periodontitis (Clark, 2017).

There are over 700 species of bacteria in the oral cavity, and a person is at risk for decay

at any given time. The predominant bacteria in the first two days of undisturbed plaque are gram-

positive streptococci such as Strep sanguis and Strep mutans. On days 2-4 gram positive

filamentous form and slender rods are added to the colonies (Wilkins, 2017). The rods eventually

take over the cocci colonies. On days 4-7 the number of filaments grows, and the flora becomes

more and more mixed as rods, filamentous forms, and fusobacteria are present. Gram-negative

spirochetes and vibrios and now detectable as the plaque near the gum line begins to thicken. On

days 7-14 vibrios and spirochetes continue to grow and cause the white blood cells in the area to
increase and inflammation becomes visible. On days 14-21, bacteria are becoming more

aggressive and densely compacted, and gingivitis can be observed in the oral cavity. The

maximum amount of plaque is reached in about 30 days, and detectable amounts of plaque can

be measured within one hour. Microorganisms existing in a matrix or biofilm are resistant to

antibiotics, antimicrobials, and to the immune system of the host organism (Overman 2017).

Disturbing the biofilm at least once ever 24 hours (brush and floss) can prevent the advancement

of dental disease (Clark, 2017).

Biofilm left undisturbed in the oral cavity can lead to various diseases, one of which is

dental caries. Caries or tooth decay is an infectious disease that can affect almost everyone. It is

characterized by the demineralization of the enamel, dentin, and cementum (Wilkins 2017).

People with increased risk for caries include those harboring cariogenic bacteria in the oral

cavity, poor oral hygiene practices, those with low saliva flow, and consumption of a cariogenic

diet (CDC, 2001). The process of demineralization requires specific criteria such as a susceptible

tooth surface, cariogenic bacteria, and cariogenic foodstuff. These things combined with the

factor of time can eventually lead to decay or cavities. Demineralized occurs when cariogenic

food (mainly sucrose or table sugar) is taken in the biofilm present in the mouth. Once the

sucrose is taken in, the pH of the plaque begins to drop and subsequently forms an acid. This

combined with frequent exposures of the tooth surface to acid will lead to demineralization and

with time a carious lesion or cavity on the adjacent crystal surface of the enamel. That being

said, bacterial plaque has a direct influence on the caries process and demineralization of the

tooth structure. The specific bacteria involved are Strep mutans, Strep sobrinus, and

Lactobacilli—these microorganisms initiate the caries process (Wilkins, 2017). The composition

of a person’s diet can also have an effect on the caries process as well as the frequency of eating
throughout the day. Sugar and sweets are usually the first to be blamed for cavities, but less

obvious culprits can also have a profound influence on demineralization. Any fermentable

carbohydrates (or foods that reduce the pH of biofilm to 5.5 or less) such as fruit, crackers,

bread, chips, cereal, and alcohol also contribute to the caries process. Additionally, the frequency

of snack and meals will increase the likelihood of decay as the tooth surface is exposed to acid

attacks multiple times a day (Carroll, Schierling, Stegemen). Fortunately, this process is

reversible. Daily brushing for two minutes (using the Bass technique—brushing at a 45 degree

angle toward the gum line) and flossing using the “C-shape” technique can be enough to disrupt

the bacterial colonies and prevent them from communicating (Clark, 2017). Consumption of

fluoridated water and the usage of topical fluoride can arrest the caries process and remineralize

the enamel in the early stages of the caries process. Fluoride is attracted to calcium and is readily

taken in by the enamel establishing an improved crystal structure (CDC, 2001). In addition,

consuming a diet fewer in fermentable carbohydrates and eating fewer times per day will have a

positive effect on acid erosion (Carroll, et al.).

Calculus is defined as mineralized biofilm and can occur supragingivally on the clinical

crown of the tooth as well as subgingivally. It is composed of calcified biofilm (minerals such as

calcium and phosphorus) and forms as a hard, tenacious mass on various surfaces in the mouth

(Clark, 2017). Supragingival calculus is white or yellow in color, is relatively hard, and may

extend past the margin of the gingiva. Saliva provides the source of minerals necessary for

supragingival calculus to form. Subgingival calculus is brown, green, or black; brittle, and

adhered to the root surface below the gum line. The mineral source for subgingival calculus is

received from gingival crevicular fluid (Wilkins, 2017). It materializes when bacterial plaque is

left in the oral cavity for more than 24 hours and it is impossible to remove with a toothbrush—it
must be scaled by a hygienist making regular cleanings incredibly important. Calculus does not

directly cause any dental diseases such as caries, gingivitis, or periodontitis. It can influence the

advancement of certain conditions, but it is never the root cause. The existence of calculus on the

tooth surface, however, supplies a prime texture and environment for new plaque to adhere, thus

contributing to the harbor of infectious bacteria. It can also contribute to periodontal infections

and pocket formation increasing the risk for periodontal disease by helping the gingiva to pull

away from the teeth. This leaves room for additional plaque to harbor in deep, hard to reach

areas. Good oral hygiene and regular visits to the dental office are ways to aid in calculus

prevention. Additionally, anti-calculus or anti-tartar toothpastes can be used to control the

formation of calculus (Clark, 2017).

Gingivitis is often a consequence of inadequate oral hygiene and is caused when biofilm

is left undisrupted on the surface of the tooth. It is a disease characterized by the inflammation of

gingival tissue made evident by redness, swelling, exudate, and bleeding upon probing. Healthy

gingiva is pale pink, firm, flat and scalloped, often stippled, and fills the space between teeth.

Health probing depth is usually between 1-3 mm. Gingivitis is often unrecognized and unnoticed

in early stages, and it is entirely reversible. With a positive change in hygiene habits, healthy

gingiva can return within a few days (Wilkins, 2017). It can vary in severity and is classified by

three stages. Stage one (or sub clinical stage) is the first few days of development of plaque and

can be recognized by dilated blood vessels (inflammation). Swelling then occurs by plasma

leakage into the surrounding tissue. Leukocytes collect in the tissue and move into the plaque

causing pus or exudate. Infection begins to increase as the collagen degrades. However, these

symptoms are not necessarily evident clinically (Clark, 2017). Stage two (or early stage) begins

4-7 days after the buildup of plaque and can continue for 21 days or more. Redness and swelling
continue to increase as well as exudate and gingival crevicular fluid. White blood cells increase

under the epithelial layer of the sulcus in the connective tissue. Collagen continues to break

down and inflammatory cells begin to spread throughout the tissue. Bleeding upon probing is

now evident clinically. Stage three (or established gingivitis) occurs after 15-21 days of plaque

buildup. Plasma cells, white blood cells, and capillaries proliferate as tissue continues to break

down. Pockets extend towards the roots and get deeper, and exudate and redness become more

visible. This stage may last months or even years but is still entirely reversible. Seven days of

proper brushing and flossing at home can reverse the effects of gingivitis. While it does not

always progress to disease, gingivitis left uncared for can lead to periodontitis (Clark, 2017).

Periodontal disease is defined as a set of diseases that are infectious and transmissible and

caused by bacteria in the biofilm collected on the tooth surface due to insufficient oral hygiene. It

is preceded by gingivitis and can consist of inflammation, increased probing depth, clinical

attachment loss, and bone loss (Clark, 2017). There is a significant correlation between

periodontal infections and several systemic conditions such as cardiovascular disease, diabetes,

respiratory disease, obesity, and rheumatoid arthritis to name a few, so it is imperative that

periodontal disease is identified, arrested, and controlled. Educating the patient of these risks is

critical in achieving compliance of proper home care. Risk factors include tobacco use, diabetes

mellitus, stress, and various medications. Occasionally, a genetic predisposition can increase

susceptibility for disease. Periodontal disease can be broken into stages much like gingivitis. The

first stage (initial lesion) is very similar to the first stage of gingivitis, in that there is little

clinical evidence of infection as the inflammatory response begins to ramp up in the first 2-4

days of bacterial accumulation. Slight marginal redness and fluid collection may be visible as the

infection progresses (Wilkins, 2017). The second stage (or established lesion) is characterized by
fluid and white blood cells infiltrating the tissue causing breakdown of collagen and increased

probing depth. Inflammation is clearly visible as is bleeding on probing and the appearance of

spongy gingiva. In the third stage (or advanced lesion) bacteria spread to subgingival biofilm

farther and farther as the pockets deepen. The immune response causes alveolar bone loss by

stimulating osteoclast activity. Connective tissue continues to degrade progressively and the

junctional epithelium becomes more and more detached (Wilkins, 2017). Clinical characteristics

of advanced stage periodontitis are mobility, bone loss, and pocket formation. It is non-

reversible, but treatment such as scaling, root planing, surgery, medication, and committed home

care are essential to management of the disease (Clark, 2017).

In summary, bacterial plaque is the direct cause of all dental diseases and conditions.

Caries, gingivitis, and periodontal disease all develop because of the inadequate removal of

plaque from the surfaces of the oral cavity through home care and regular professional cleanings.

Calculus does not cause disease, but creates a hospitable environment for plaque to adhere to and

proliferate. It requires commitment and compliance from the patient, but brushing and flossing

with proper technique for two minutes at least once a day, consuming a responsible diet low in

cariogenic food and drinks, and regular dental cleanings is imperative to controlling and

preventing dental disease.

 References

Carroll, D., Schierling, J., Stegeman, C. The Battle of the Fermentable Carbohydrates. Retrieved
from https://talon.kirkwood.edu/d2l/le/content/60623/viewContent/1784872/View

Clark, S. (2017). Preventive Dentistry [PDF Document]. Kirkwood Community College.

Retrieved from
https://talon.kirkwood.edu/d2l/le/content/60623/viewContent/1797762/View

Overman, P. Biofilm: A New View of Plaque. Retrieved from https://www.dentalcare.com/en-

us/professional-education/ce-courses/ce42/toc

US Department of Health and Human Services. Centers for Disease Control and Prevention
(CDC). (2001). Recommendations for using fluoride to prevent and control dental caries
in the United States. (Morbidity and Mortality Weekly Report, Vol. 50, No. RR-14)
Retrieved from https://stacks.cdc.gov/view/cdc/5160

Wilkins, E. (2017). Clinical Practice of the Dental Hygienist. Philadelphia, PA: Wolters Kluwer.