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Stefanie Fischer
Preventive Dentistry Research Paper
November 19th, 2013
Bacterial Plaque and Its Relation to Dental Diseases
Bacterial plaque, is a dense, nonmineralized, complex mass of colonies in a gel-like
intermicrobial matrix, (Wilkins 2013). It is generally composed of microorganisms and an
intermicrobial matrix, of which approximately 80% is water and 20% is organic and inorganic
solids. The composition of bacterial plaque varies from mouth to mouth. Bacterial plaque forms
on teeth in five distinct stages. First, pellicle forms on a tooth surface which is followed by
attachment of bacteria onto the pellicle. Bacteria are able to colonize and multiply once they
have attached to the pellicle. If the bacteria are not disturbed, they are then able continue
growing and maturing. The last step is formation of the matrix, which is derived mainly from
saliva for supragingival biofilm and from gingival sulcus fluid and exudate for subgingival
biofilm, (Wilkins 2013). Bacterial plaque is the culprit of much pathology within the mouth,
especially inflammatory dental diseases. Its presence signals the beginning of dental caries as
well as gingivitis and, finally, periodontal disease. Bacterial plaque is also the foundation of
calculus formation since, Calculus is essentially mineralized dental biofilm, (Wilkins 2013).
(Clark 2013).
The dominant bacteria vary throughout the maturation of bacterial plaque. Days one and
two, gram positive cocci, such as Streptococcus mutans and Streptococcus sanguis, dominate the
bacterial makeup of plaque. The cocci are still present in the largest numbers on days two
through four, however; slender rods and filamentous forms of bacteria begin to show. The

filamentous forms continue to grow in number on days four through seven and the composition
of the bacteria differs even more. This time period is where we begin to see gram negative
bacteria appear as well as see bacterial plaque thicken at the gingival margin. Days seven to 14
are where the gram negative vibrio and spirochete forms show up. Here there is an increase of
gram negative organisms, anaerobic organisms and white blood cells along with gingival
inflammation. Days 14 to 21 are when the present bacteria begin to organize and orient
themselves perpendicular to the tooth surface and gingivitis becomes obvious to the clinician.
(Clark 2013).
Caries is a disease of the hard tooth structures which causes cavities through a process of
demineralization. Three things are necessary for the caries process: a tooth, cariogenic material
and microorganisms. Bacterial plaque is composed of layers of organized bacteria, or
microorganisms. In order for caries to occur, plaque must be present in the mouth. The bacteria
involved in the formation of caries are lactobacilli and acid-forming bacteria such as S. mutans
and Streptococcus sobrinus. (Clark 2013).
The initial infection is initiated by ingested cariogenic food which creates bacterial
plaque over time. When more cariogenic food is eaten, acid is produced by bacteria that digest
those food particles. These acids, in turn act to demineralize the enamel, cementum, and/or
dentin, (Wilkins 2013). The acid is able to diffuse through microchannels of the enamel and
begin demineralization, creating a subsurface lesion that is generally invisible. Demineralization
occurs when minerals, such as calcium and phosphorus, are removed from the tooth by the acids
in the mouth. At this point, demineralization continues on the subsurface layer of enamel and the
subsurface lesion develops into a white spot lesion. Since remineralization is possible at this
point in the process, care must be taken not to scratch at the demineralized surface with any

hygiene instruments. As a later stage white spot lesion, there is still a chance for remineralization
to reverse caries. Remineralization is when minerals are deposited back into the tooth surface. If
a later stage white spot lesion doesnt have the opportunity to remineralize, the lesion progresses
to a cavitated lesion. Dietary factors of food such as texture, cariogenicity, retentiveness,
frequency and amount are among some of the factors that play a large role in the process of
caries. Frequency is one of the most important factors in that list. The less often cariogenic foods
are eaten, the better for teeth because the pH in the mouth has time to reset itself. If cariogenic
foods are eaten frequently through the day, the pH has no time to return to neutral and the acid
formed from those foods is constantly attacking the enamel. (Clark 2013).
Calculus is, mineralized dental biofilm that is filled with crystals of various calcium
phosphates, (Wilkins 2013). Calculus is nothing but a hardened, or mineralized, version of
bacterial plaque that hasnt been disturbed from the mouth. The formation of calculus follows the
same steps of formation as plaque. Calculus first goes through a stage of pellicle formation then
a stage of plaque formation and finally the plaque is mineralized to form hardened calculus.
There are two specific types of calculus that are named according to location relative to the free
gingival margin. Supragingival calculus is found on the clinical crown of the tooth which is
located above the free gingival margin. Subgingival calculus is located on the root surface of the
tooth which is located below the free gingival margin. Supragingival calculus is most frequently
found on the lingual surfaces of mandibular anterior teeth as well as the buccal surfaces of the
maxillary molars while subgingival calculus is most frequently found in the interproximal spaces
of the teeth. (Clark 2013).
The general composition of calculus is, inorganic and organic components and
water; however, the composition of the two types of calculus vary from one another slightly

(Wilkins 2013). Inorganic material makes up a majority of the composition of calculus and
includes phosphate, calcium, calcium carbonate, magnesium, sodium, potassium, trace elements,
fluoride and crystals. Subgingival composition is essentially the same but comprised of a larger
amount of calcium, magnesium and fluoride than supragingival calculus. The clinical
characteristics of the two types of calculus also differ. Supragingival calculus is a white or gray
color, is amporphous in shape and is moderately hard. Subgingival calculus can by varying
shades of brown, dark green or black, is flattened to fit into the pocket wall of the tooth and is
brittle and harder than supragingival calculus. (Clark 2013).
Calculus plays, an important role in the development, promotion, and recurrence of
gingival and periodontal infections, (Wilkins 2013). Calculus itself doesnt cause periodontal
disease, it merely gives bacterial plaque the perfect rough surface to attach to and grow on. When
the bacteria can collect and stick easily on a surface in the mouth, it increases the likelihood of
increased pocket depth as well. The larger the pocket depth, the more room bacteria has to grow
in the mouth. The true culprit of periodontal disease is bacterial plaque; calculus merely provides
the ideal environment for bacteria. (Clark 2013).
Gingivitis is, inflammation of the gingival tissues, (Wilkins 2013). This disease occurs
when plaque, made up of layers of bacteria, is present in the mouth. Some clinical signs of
gingivitis are exudate, redness, swelling, and also bleeding on probing. After an initial irritation
from bacterial plaque, the body sends an inflammatory response to get rid of the bacteriathis is
the first stage of gingivitis. Lymphocytes are present and edema in the tissues is caused by
plasma in the spaces of connective tissue. Aside from minor edema, there are no other clinical
signs of gingivitis yet. In stage two there is an increase in the breakdown of collagen fibers,
exudate, and T-lymphocytes in the connective tissue. Here we may see red and swollen tissue

which bleeds on probing. In the final stage of gingivitis, we see continued destruction of collagen
fibers, thick junctional epithelium and pocket formation. We also see a dominance of plasma
cells as well as an equal amount of T-lymphocytes and B-lymphocytes. At this stage there is
obvious inflammation and redness of the gums and an increase in the amount of exudate.
Gingivitis can be reversed at any of the three stages by oral health care and removal of bacterial
plaque; however, if nothing is done to reverse this disease it will develop into periodontitis in
most cases. (Clark 2013).
Periodontitis is, inflammation in the periodontium affecting gingival tissues, periodontal
ligament,cermentum, and supporting bone, (Wilkins 2013). Plaque, or more specifically a,
shift in plaque bacteria, causes periodontitis (Clark 2013). When bacterial plaque is below the
gum line it is referred to as subgingival biofilm. Once bacterial plaque reaches the subgingival
level it produces toxins that irritate the tissue of the gums. The body responds to these toxins
with an inflammatory response in an attempt to get rid of the toxins. (Clark 2013).
In the process of getting rid of the invaders, the body also begins to destroy alveolar bone
within the gums. As the body destroys more bone and connective tissue fibers, the gums
themselves begin to pull away from the teeth, creating a periodontal pocket. The pockets create
more space for bacterial plaque which creates further toxins and signals the body for a larger
inflammatory response, removing more bone and structure from the gums in the process.
Periodontal disease is one large circle of destruction that cannot be reversed, only kept in check.
(Clark 2013).
The main goal of a dental hygienist is to prevent periodontal disease because it is
irreversible. Caries, calculus and gingivitis are all reversible with good professional treatment

and continued homecare. Control and elimination of bacterial plaque is the one thing that helps
to prevent each and every one of the oral diseases discussed in this paper. With simple daily oral
hygiene of brushing and flossing to remove bacterial plaque, there would be no caries, calculus,
gingivitis or periodontal disease. (Clark 2013).

Works Cited
Clark, S. (2013). Dental Hygiene Notes. KCC.
Clark, S. (2013). Preventive Dentistry Notes. KCC.
Types of Gum Disease. Retrieved from http://www.perio.org/consumer/types-gumdisease.html#OverlayWrapper[flash]/0/
Wilkins, Esther. (2013). Clinical Practice of the Dental Hygienist. Philadelphia, PA:Lippincott
Williams & Wilkins.
Wright, J. Timothy. (2010). Fighting Caries with Remineralization. Dimensions of Dental
Hygiene. 8 (2). Retrieved from
http://www.dimensionsofdentalhygiene.com/2010/02_February/Features/Fighting_Caries
_with_Remineralization.aspx