Preventive Dentistry Research Essay
19 November 2013
Plaque is the Culprit
Oral health care such as brushing and flossing are typically advised habits to keep our mouths “clean”. Blah, blah, blah. Here is a concept that patients will be interested in; bacteria growing on their teeth! Bacteria are everywhere and as a result of providing a stable, moist, warm environment oral bacteria can multiply and structuralize into plaque right in their mouths. Plaque is as unattractive cosmetically as it is to oral health. Most patients associate that plaque can cause cavities of the tooth, but plaque can affect much more. If not managed correctly plaque can be the cause of caries, calculus, gingivitis, and periodontitis.
It is common knowledge that bacteria are everywhere. Good bacteria and bad are thriving continuously on surfaces and even in our bodies. Bad bacteria are inevitable to avoid, however, they are manageable and significant amounts can be prevented. Prevention and management of oral bacteria and its affects are objectives of dental hygienists. Humans begin retracting bacteria into their mouths soon after birth and throughout their lives. When oral bacteria are provided a suitable and “comfortable” environment in the mouth they begin metabolizing and thriving there to become bacterial plaque. Bacterial plaque is a densely organized bacterial system. It all begins when glycoproteins are absorbed onto dental enamel to form a bacterial, thin, membranous pellicle over the tooth surface (Wilkins 2013). Then selective colonization of the pellicle by microorganisms occurs resulting in the growth and maturation of plaque. Said pellicle is acquired just twenty minutes following brushing. Then, bacteria attach to the pellicle and begin multiplication and colonization (Clark 2013). If left undisturbed in just two weeks’ time the bacteria has altered from predominant streptococci to include vibrio and spirochetes, the body has activated defense mechanisms, and the gingiva has become inflamed to near gingivitis (Todar 2012). While bacterial plaque is making a home on the teeth it also presents this pathological potential. The tissues surrounding tooth structures do not tolerate bacteria well. This can apply when bacterial plaque is present on the tooth surface and the gingiva become irritated and begin migrating away. These significant changes can progress into diseases of the hard and soft oral cavity tissues such as teeth, bone and gingiva, and cause gingivitis or periodontal disease if left untreated (Wilkins 2013).
Caries are a bacterial chemical reaction created by means of food, bacteria and tooth structure. Plaque contributes to the formation of caries because it consists of microorganisms that metabolize substances and cause a shift in acidity within the oral cavity. That acid immediately diffuses through micro channels between enamel rods on the surface of teeth and begins destroying structures. This effect comprises the first stage of dental caries. Without correctional action a stage two white spot lesion may form and if the neglect continues the tooth surface will demineralize and results in cavitation (a cavity) (Clark 2013). The six categories of caries are as follows; acute, rampant, chronic, recurrent, arrested and incipient. Acute is rapid destruction of tooth surfaces. Rampant accounts for nearly all surfaces being affected. Chronis is the slow progression of only a few superficial teeth. Recurrent lesions recur around previously restored lesions. Arrested are the slowing or stopping of developing lesions. And incipient caries only affect the enamel (Fotek 2012). There are other factors which can affect the production of caries and are quite manageable such as diet, time, acidity, and frequency. Caries risk can be reduced by opting for a less cariogenic diet with less sucrose and acid. Limiting exposure time of the teeth to any bacterial metabolizing can help too by allowing the oral pH to recover after consumption instead of sustaining a level necessary to metabolize by snacking frequently.
When bacterial plaque begins to deposit calcium and phosphate salts it develops into calculus. This hardening creates a tenacious material on the tooth surfaces above or below the gingival margin. Calculus is composed 70-90% inorganic materials, phosphate, calcium carbonate, magnesium. Supra gingival calculus can be found on the clinical crowns of teeth, especially on the lingual mandibular anteriors and buccal of maxillary first and second molars appearing in white, yellow, and tan sheets (Clark 2013). Sub gingival calculus is found most commonly on the interproximal surfaces and generalize throughout the mouth as tenacious, black or dark green, in ridges or ledges. Sub gingival calculus attaches itself to the tooth structure by the calcium and phosphate crystals growing into cemental irregularities of the surface (Clark 2013). It originates as a pellicle which cultivates into plaque and then alters by mineralization into calculus. If left to mature, calculus can cause gingivitis, periodontal infection and even pocket formation (Wilkins 2013). Calculus does not, however, cause periodontal disease; plaque does.
When bacterial plaque is present on the tooth surface the surrounding gingiva respond by becoming enflamed and deviating from normal without attachment loss. This bodily response to plaque is known as gingivitis. It begins at stage one; the initial and subclinical acute inflammatory response of the gingiva. This initial stage is characterized by the blood vessels dilating, PMN’s attaching to vessel walls and migrating into surrounding tissues, plasma leaking into the surrounding connective tissue (edema), and an increase in lymphocytes (Clark 2013). Thus progressing to stage two where there is an increase in T-lymphocytes, the formation of exudate, and the tissues appearing slightly red and swollen. Later in this “early stage” of gingivitis the collagen fibers are destroyed giving way to the loss of stippling. In addition, the junctional epithelium begins to elongate and there is evident bleeding upon probing. Lastly, during the “established stage” of gingivitis the cellular makeup has changed by plasma cells becoming predominant, T and B-lymphocytes equal in numbers with B-lymphocytes releasing lyphokines to accelerate tissue destruction, the epithelium thickening and extending further apically, and blood vessels proliferating into capillaries. Externally, note the visible pus as well as the gingiva appearing red due to this capillary proliferation (Wilkins 2013). These are the stages and events of gingivitis and it is a dental hygienist to note color change, edema, exudate and hemorrhage. Of course we can prevent such a destructive disease by practicing good hygiene habits. Miraculously, all can be restored by the same means. Healing of gingivitis advances in the reverse of pathogenesis (Clark 2013).
It is important to recognize the initiator of this disease as dental plaque. This plaque can originate from lack of consistent oral hygiene care and more probable with local contributing factors such as malposed teeth, dental restorations, and orthodontic appliances (Wilkins 2013). In addition, there exist many biochemical factors that can contribute to the instigation of gingivitis as well; some examples include stress, hormones or medications.
One last major oppressor of the dental hygiene world is periodontitis. Periodontitis is a set of periodontal diseases characterized by clinical attachment loss, alveolar bone loss, increased probing depth and gingival inflammation (Periodontitis 2013). This ailment too is in relation to plaque because it is
preceded by gingivitis. First plaque inflames the surrounding gingiva eventually evolving into gingivitis. Then a shift in plaque bacteria occurs and the immune system facilitates by prompting inflammatory destruction of periodontium. Clinical signs of this endeavor are a bluish/red coloring of tissue, deepening sulci, reabsorption of bone, decreased stippling, edema, bleeding on probing and instrumentation, pocket formation and mobility (Clark 2013). A radiograph is necessary to legitimately diagnose perio. In basic terms, the patient has allowed plaque to accumulate on the tooth surface, the gingiva have responded to the endotoxins released by plaque with inflammation, and consequentially if improvements have not been made the gingiva and supporting structures will begin to recede apically away from the plaque. This in turn affects all supporting structures surrounding the affected areas including the alveolar bone. Periodontitis can be classified as chronic, slight, moderate, or advanced depending on documented clinical attachment loss. Chronic periodontitis is characterized by gradual clinical bone loss mainly horizontal in nature. Slight, moderate and advanced classes are established by probe depth plus recession. Slight is one to two millimeter loss, moderate is three to four, and advanced is loss of more than 5 millimeters. Plaque is a major contributor to the development of periodontitis, but there are a few systemic factors that act as contributors as well such as diabetes, HIV/AIDS, osteoporosis, pre-term low birth weight babies, and bacterial pneumonia (Clark 2013). Beyond the clinical aspects, a patient with periodontitis should be advised that if left untreated symptoms can include root caries, root sensitivity, tooth loss/mobility, and damage once done is non-reversible. Treatment of periodontitis is more or less exploiting professional care and homecare in hopes of maintaining the current state and preventing more degeneration.
Now that the chief clinical features of less than effective oral health care have been discussed, how can a patient avoid such ailments? Prevention is the humble solution. First, a point must be made in what lies at the center of this oral disorders web; it is plaque or more simply bacteria. Plaque forms when bacteria begin to accumulate and organize, therefore it is enforced that a patient take steps to prevent this by stirring and disorganizing any bacteria on our tooth surfaces every twenty-four hours or so. This can be accomplished by utilizing a toothbrush with proper technique to scrub all tooth surfaces as well as sweep subgingivally. Toothpaste is a great addition to this practice because it offers abrasive particles to better scrub away bacteria, it contains fluoride which fills enamel tubules preventing harmful toxins from filling them instead, and it helps lubricate surfaces so brushing is more comfortable. Floss is an excellent aid in prevention of bacteria and plaque buildup because it can remove cariogenic substances from hard to reach interproximal spaces. This way the particles will not remain and begin metabolizing harmful toxins. The particles ingested can also play a role in prevention. By avoiding cariogenic foods such as ones that are acidy or contain sucrose the intensity of surface exposure is reduced. Reducing that exposure time is helpful as well. Rather than sipping and snacking multiple times and therefore initiating the toxin metabolizing, arrange meals accordingly. In those meals you can also include more fluoride by consuming fluoridated water or foods that contain it. Water also happens to be a brilliant matter to swish vigorously in the oral cavity to dislodge food particles, wash away even smaller particle from the tooth surface, and if fluoridated it can introduce fluoride into the enamel tubules.
For such intimidating consequences of not practicing oral health care, the care itself is quite simple, inexpensive and yet significant. Agitate the bacteria once a day by brushing and flossing. Avoid aiding its metabolizing by limiting consumption exposures and acidity. Also introduce fluoride to tooth surfaces when possible. And lastly, seek professional care regularly to resolve issues beyond homecare and to ensure your oral health.
Clark, S. (2013) Preventative Dentistry Notes, KCC.
Fotek, P. National Institutes of Health, U.S. National Library of Medicine. (2012). Dental cavities. Retrieved from website: http://www.nlm.nih.gov/medlineplus/ency/article/001055.htm
Periodontitis. In (2013). Wikipedia, the free encyclopedia. Retrieved from http://en.wikipedia.org/wiki/Periodontitis
Todar, K. (2012). The normal bacterial flora of humans . Retrieved from http://textbookofbacteriology.net/normalflora_3.html
Wilkins, E. (2013). Clinical practice of the dental hygienist. (11 ed.). Philadelphia: Wolters Kluwer.