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One of the strongest correlations between periodontal disease and another disease that could have heavy implications as to whether periodontal disease progresses is the correlation and relationship between diabetes and periodontal disease.
A recent study determines that "the prevalence of diabetes mellitus (DM) and periodontal disease/periodontitis (PD) is high, and the association of these two as risk factors influencing each other has been recognized and is extensively documented" (Acharya, Satyanarayan, Thakur, 2010, p. 70). This is another disease that is correlated to periodontal disease, and with that correlation is additional evidence that gingivitis does not always preclude the more destructive form of periodontal disease. Many periodontal therapists have for the last few years known and espoused the fact that patients who took care of their oral health faced far fewer health related challenges than those that did not. One 2002 study professed "health professionals need to be cognizant of the effect dental health can have on systemic diseases and refer for treatment when appropriate to ensure that optimum oral and systemic health is achieved for their patients" (Greenwell, Bissada, 2002, p 2581). Another study showed how "poor oral hygiene, gingivitis and periodontal disease are the most important risk factors for the development of white spot lesions" (Noble, 2008, p. 25). Still another study was undertaken to determine what effect, if any, daily treatment would have on the occurrence of gingivitis with the results being as what many expected. The study found that "gingivitis is often caused by inadequate oral hygiene, which leads to plaque buildup" (Type, 2008). If it were true that gingivitis always leads to periodontal disease, then it is probably safe to assume that the health of a person is almost always affected if the individual does not take care of his or her oral responsibilities. If the individual is taking care of their oral hygiene responsibilities then the four stages of periodontal disease progression could be alleviated.
Those four stages proceed from gingivitis "used to describe soft tissue inflammatory changes" (Bellows, 2004, p. 16) and when "periodontitis is diagnosed (when) attachment loss has occurred" (Bellows, p. 16). According to Bellows there is a grading system that allows the dentist to judge how far along the disease has progressed. Depending on how far the disease is, allows for certain treatments. If done successfully, the initial stages of periodontal disease is arrested and gingivitis then no longer proceeds to the more destructive forms of the disease. Since there are four distinct stages to periodontal disease any of which could possibly be corrected, does that not also mean that contracting gingivitis (which is very prevalent in society) does not always mean that it will progress to periodontal disease and it may also mean that periodontal disease is not always preceded by gingivitis.
The fact that many of these studies tend to confirm that many very serious diseases go hand in hand with periodontal disease is just one reason why it may be necessary to conduct additional studies to confirm or negate the thesis of this paper. With the variance of doubt playing through the available literature, more conclusive findings may be appropriate. This is especially true since periodontal disease and gingivitis can both be causes of other maladies including the fact that even newborn babies can be affected. One recent study determined that "birth weight, height, and head and chest circumference of babies born of mothers with established periodontal disease were significantly lower than those who were born of mothers with healthy periodontal condition, gingivitis and initial periodontal disease" (Shirmohammadi, Pourabbas, Bilan, Chitsazi, 2009, p. 102).
This particular study provides further evidence (though certainly not conclusive in nature) that gingivitis does not necessarily precede periodontal disease. If the birth differences were more similar than what the study showed, then one could surmise that gingivitis and periodontal disease were the precursors to the more destructive levels of periodontal disease. However, since the numbers are so dissimilar, many experts could point to the findings and say that such numbers allow for some leeway regarding the question at hand.
Another study determined that an even slighter difference in gingivitis and the more advanced form of periodontal disease might be examined. The study found that the "autoimmune response to HSP60 may exert in periodontitis lesion, and suggest that perhaps subtle differences in the balance of cytokines may result in different disease expression" (Honda, Domon, Okui, Kajita, Amanuma, Yamazaki, 2006, p. 35). Knowing that a cytokine imbalance might be the source behind whether an individual develops gingivitis or the more destructive form of periodontitis might be the key to unlocking the secrets of periodontal progression. It might also provide evidence that certain cytokines not associated with gingivitis might be the reason(s) behind such progression. It might be that not only do certain cytokines reside in the gingival connective tissue, but that the plaque that builds up in those same areas is the primary source of inflammatory reactions that can bring about periodontal disease. One study that looked at the relationships of gingivitis, cytokines and other bacterial-associated gingival found that "with accumulation of plaque on teeth, it appears that a bacterial stimulus induces the expression of MCP-1 in mononuclear phagocytes and endothelial cells" (Graves, 1999, p. 482).
If it is true that the MCP-1 induces inflammatory responses then the protein found in those cells could be a source of concern regarding the progression of gingivitis. Monocyte attraction of the protein profoundly affects the gingival connective tissue.
The available literature abounds with examples and studies showing the connections (slight and otherwise) between periodontal disease and gingivitis. At the same time it also shows connections between, diabetes, pregnancy, smoking and non-smoking, obesity, gingivitis and the most destructive form of periodontitis. There are far too many of these connections to ignore, and far too many connections to conclusively state that gingivitis always precedes periodontal disease. Many experts may be able to point to this study or that in order to provide evidence of their particular stance, however, the wide myriad of available literature does not conclusively evidence any particular stance or viewpoint. The literature does provide a number of avenues of discovery as well as a number of contemplative ideas and thoughts for the researchers following the problem of progressive periodontal disease. Many experts have professed their own viewpoint and at the very least has provided academia with a problem that individuals can certainly sink their teeth into.
Academy report (2003) American Academy of Periodontology, Report 74, pp. 1 -- 9
Acharya, A.B.; Satyanarayan, A.; Thakur, S.L.; (2010) Status of association studies linking diabetes mellitus and periodontal disease in India, International Journal of Diabetes in Developing Countries, Vol. 30, Issue 2, pp. 69-74
Aschmwanden, C. & Chen, I.; (1998) How to keep your smile, Health (Time Inc. Health), Vol. 12, Issue 7, p. 22
Bellows, J.; (2004) Periodontal disease -- a primer on recognition and therapy, DVM: The Newsmagazine of Veterinary Medicine, Vol. 35, Issue 1, pp. 16S -- 24S
Costerton, J.W.; Stewart, P.S.; Greenberg, E.P.; (1999) Bacterial biofilms: a common cause of persistent infections, Science, Vol. 284, pp. 1318-1322
Dye, B.A.; Kruszon-Moran, D.; McQuillan, G.; (2002) The relationship between periodontal disease attributes and helicobacter pylori infection among adults in the United States, American Journal of Public Health, Vol. 92, Issue 11, pp. 1809 -- 1815
Graves, D.T.; (1999) The potential role of chemokines and inflammatory cytokines in periodontal disease progression, Clinical Infectious Diseases, Vol. 28, Issue 2, p. 482
Greenwell, H. & Bissada, N.F.; (2002) Emerging concepts in periodontal therapy, Drugs, Vol. 62, Issue 18, pp. 2581 -- 2587
Honda, T.; Domon, H.; Okui, T.; Kajita, K.; Amanuma, R.; Yamazaki, K.; (2006) Balance of inflammatory response in stable gingivitis and progressive periodontitis lesions, Clinical & Experimental Immunology, Vol. 144, Issue 1, pp. 35-40
Hullah, E.; Turok, Y.; Nauta, M.; Wai Yoong; (2008) Self-reported oral hygiene habits, dental attendance and attitudes to dentistry during pregnancy in a sample of immigrant women in North London, Archives of Gynecology & Obstetrics, Vol. 277, Issue 5, pp. 405 -- 409
Marquis, R.E. (1995) Oxygen metabolism, oxidative stress and acid-base physiology of dental plaque biofilms, Journal of Ind Microbiology, Vol. 15, pp. 198-207
Meta-analysis of peridontal disease and risk of coronary heart disease and stroke (2003) Current Medical Literature: Stroke Review, Vol. 7, Issue 3, p. 77
Milone, A.; (2008) Does periodontal disease cause Type 2 diabetes?, Endocrine Today, Vol. 6, Issue 20, pp. 1-14
Noble, J.; (2008) Out damned spot!, Vital, Vol. 5, Issue 3, p. 25
Page, R.C. & Schroeder, H.E (1976) Pathogenesis of inflammatory periodontal disease: A summary of current work, Lab Invest, Vol. 34, Issue 3, pp. 235-249
Paunica, S.C.; Dumitriu, A.; Mogos, M.; Georgescu, O.; Mogos, I.; (2009) The evaluation of the periodontium in patients with leukemia using thermographic imaging, Hematology, Vol. 14, Issue 6, pp.…[continue]
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Nevertheless, an individual may prefer to have this type of calculus removed for other reasons or otherwise as part of a long-term treatment regimen. For example, Bennett and Mccrochan note that, "When the American Dental Association later approved Warner-Lambert's mouthwash, Listerine, by stating that 'Listerine Antiseptic has been shown to help prevent and reduce supragingival plaque accumulation and gingivitis. . ., ' sales rose significantly" (1993:398). It remains unclear,