This is definition of my topic: “Periodontal disease is defined as an inflammatory disease of the supporting tissues of the teeth caused by specific microorganisms or groups of specific microorganisms, resulting in progressive destruction of the periodontal ligament and alveolar bone with increased probing depth formation, recession, or both” (Aguirre, Newman, & Takei, 2015, p. 50-51). To further explain what periodontal disease might look like in a clinical setting, imagine red/purple swollen gums, which are usually tender to the touch and bleed when probed, as well as some recession (bone loss) contributing to tooth mobility, and in really severe cases, puss (from infection). It is important to understand that this disease does not occur overnight, but actually over years of unhealthy habits. The following is a small summary of different stages leading to periodontal disease from the microbiologist perspective of Bauman & Primm (2018):
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Hard deposits of called tartar or dental calculus form when calcium salts mineralize plaque. Tartar trapped at the base of the teeth trigger the initial form of periodontal disease —gingivitis. Swelling of the gums, plaque, and tartar can also form oxygen-free pockets that become colonized by anaerobic bacteria, such as Porphyromonas gingivalis, compounding the infection and producing a condition called periodontitis. P. gingivalis produces five protein-digesting enzymes that break down gingival tissue. Further destruction occurs as bacteria invade the bone, causing osteomyelitis (inflammation of the bone marrow and bone), and teeth become loose and fall out (pg. 713).
This disease progresses slowly over many years, but the initial signs and symptoms to clinically show would be red, swollen, tender, bleeding gingiva also known as gingivitis. Gingivitis is caused by a multiple of microorganisms making your mouth their home to thrive in. Bacteria can grow and survive in many different environments, but the human mouth is especially good for bacteria because it is continuously moistened with saliva, nutrients pass through as food, and can be very hard to keep clean. Not to mention, there may be some behavioral factors of the host that aid the survival of microorganisms such as stress or smoking. We make it very comfortable for hundreds of species of bacteria to thrive, especially at the cemento-enamel junction (CEJ) which is where the crown of the tooth meets the roots.
The best survival technique used by these bacteria is their creation of what it called a biofilm (can also be referred to as slime layer). Here is a short microbiological description, from Bauman & Primm (2018), of how a dental plaque biofilm is formed:
Plaque formation usually begins with colonization of the teeth by Streptococcus mutans. This bacterium breaks down carbohydrates, particularly the disaccharide sucrose (table sugar), to provide itself with nutrition and a glycocalyx. One of its enzymes catabolizes into its component monosaccharides – glucose and fructose – which the cells use as energy sources. A second enzyme polymerizes glucose into long, insoluble polysaccharide strands called glucan molecules, which form a sticky matrix around the bacteria. Glucan adheres S. mutans to the tooth, provides a home for other species of oral bacteria, and traps food particles. A biofilm has formed (p. 169).
At this point, normal brushing and flossing are not strong enough to remove the biofilm that has been created. Seeing a dental hygienist for a teeth cleaning is very important because he/she can manually scrape away this plaque build-up. As mentioned earlier in the description of progression, the biofilm allows for air-tight pockets to form, and if untreated, introduces a new irreversible threat: potential infection and bone loss.
The bacteria are now attached to the teeth and are growing, unscathed by normal brushing and flossing. The host body immune system takes on the fight by sending the blood into the tissues to deliver polymorphonuclear leukocytes (neutrophils), lymphocytes, and plasma cells (Aguirre et all., 2015, p. 220). Unfortunately, the body’s defensive mechanisms are no match for the defensive system of the bacterias’ biofilm but instead can be harmful to the host’s own tissues. “More recently, it was established that the host’s immunoinflammatory response to the initial and persistent bacterial attack unleashes mechanisms that lead to collagen and bone destruction” (Aguirre et all, 2015, p. 279). As the body’s immune system gets involved to try and fight off the bacteria, in turn the tissues and bone surrounding the bacteria is being destroyed. Gingivitis becomes more apparent clinically showing the signs such as gums that bleed when touched, inflammation, and the most prevalent is the formation of pockets around the teeth.
At this stage, if seen by a dentist, periodontal probing depths might be moderate, in the 5-7 range where as normal measurement would be 2-4. A periodontal probing measures the pocket depths around the teeth (specifically from the cemento-enamel junction of the crown, in millimeters deep) to determine how much tissue attachment has been lost and level to which the bone has dropped (caused by both the bacteria and the host’s immune response). Any measurements 8mm+ are in late stage periodontal disease and have major tooth mobility with high risk for extraction. Like any other bone in our body, when in use (relative example: mastication) normal body processes are for osteoclasts to destroy bone and osteoblasts to replace with new bone. Once teeth are mobile enough for extraction, that bone level will dramatically drop because it is no longer “being used”.
Radiographs are a major tool in diagnosing the level of bone loss a person has from periodontal disease. If bone loss is seen on the radiographs, this is a sign that the periodontal disease is past its initial stage (which can only be detected clinically) (Aguirre et all., 2015, p. 379). Bite-wing radiographs capture the crown of the teeth as well as the level of bone. Periapical radiographs capture the apex of the roots in search of any infection which would present itself as a dark, circular shadow surrounding the apex. The level of bone loss cannot be measured from radiographs alone because it can be geometrically inaccurate (for example: 2-D images can have overlap). Since periodontal disease is managed over years, it is helpful to take x-rays yearly to track any progression of bone loss.
A study was done called Influence of pH on inhibition of Streptococcus mutans by Streptococcus oligofermentans proving that Streptococcus oligofermentans can kill Streptococcus mutans by converting the lactic acid (made by the Streptococcus mutans) into hydrogen peroxide (Liu et all., 2014).
There is a specialized field of study for dentist’s who are interested in continued education to become a Periodontist. Periodontal disease is not exactly curable, but instead maintained over a lifetime.
Statistics on how many people in the united states have the disease. What age group is it most associated with?
What are the main causes of the disease? Any specific promotions of disease causing agents?
Treatment/Solution: Cost in treating the disease? What procedures are covered by insurance?
“Gingivitis occurs frequently in many people and to varying degrees over the course of one’s lifetime, though it usually first appears during puberty and early adulthood. If not treated, it leads to recurrent gingivitis or periodontal disease, which occurs in about 47% of adults ages 30 to 65 in the United States and in over 70% of people over age 65” (Bauman & Primm, 2018, p. 713).
- Aguirre, A., Newman, M. G., & Takei, H. H. (2015). Clinical Periodontology (12th ed.) (F. A. Carranza, Ed.). Philadelphia: Saunders.
- Bauman, R. W., & Primm, T. P. (2018). Microbiology: With diseases by body system (5th ed.). Upper Saddle River, NJ: Pearson.
- Ebersole, J. L., Dawson, D., Emecen-Huja, P., Nagarajan, R., Howard, K., Grady, M. E., … Dawson, D., 3rd. (2017). The periodontal war: microbes and immunity. Periodontology 2000, 75(1), 52–115. https://doi-org.westcoastuniversity.idm.oclc.org/10.1111/prd.12222
- Liu, Y., Chu, L., Wu, F., Guo, L., Li, M., Wang, Y., & Wu, L. (2014). Influence of pH on inhibition of Streptococcus mutans by Streptococcus oligofermentans. European Journal of Oral Sciences, 122(1), 57–61. https://doi-org.westcoastuniversity.idm.oclc.org/10.1111/eos.12102
- Slots, J., & Slots, J. (2017). Periodontitis: facts, fallacies and the future. Periodontology 2000, 75(1), 7–23. https://doi-org.westcoastuniversity.idm.oclc.org/10.1111/prd.12221
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