Progression of periodontal disease

Progression of periodontal disease

Primer: periodontal diseases

According to Kinane et al.(38). Periodontal disease is a wide range of conditions related to the inflammatory effects that affect the supporting structures of teeth. These structures are the gingiva, bone, and periodontal ligaments. Traditionally, periodontal disease was commonly prevalent with the aged people, but recently, researchers have shown that periodontal disease can also be present in the children (Kinane et al.,39). Chronic incidences of the disease are evident in the adults while aggressive periodontitis may also affect children or adolescents.

Smoking is the main predisposing factor for this disease. The more a person smokes, or the longer one smokes, the higher the chances of getting the disease. In case one smokes when they already have the disease, it will accelerate it, and become more severe. Smoking is controllable but there are other uncontrollable factors: genetic factors where some people are susceptible to the disease and fluctuating hormonal levels.

According to Kinane et al.(38) gingivitis can be reversed but in susceptible individuals progresses to chronic periodontitis. This is because susceptibility to gingivitis reflects susceptibility to chronic periodontitis as well. The absence of gingivitis is termed as a good indicator for long-term maintenance of periodontal health both on an individual and site-specific basis (Kinane et al,39). Another uncontrollable factor is the level of circulating hormones like estrogen (Kinane et al. 39). They might enhance gingival inflammation but they often do not increase the susceptibility to chronic periodontitis

Proper and effective treatment of the diseases mainly is enhanced by timely and accurate diagnosis. This is because, if the disease will already have progressed to the extent of loss of bones and tissues, reversing this loss is completely impossible. However, since periodontal disease in early stages is painless, patients rarely seek early care (Kinane et al. 39). The main sign of gingivitis is bleeding during tooth brushing while there is no pain reported to be present.

The cause of the disease depends on individual factors or specific gingival sites. Some individuals are more susceptible to the effects of dental plaque accumulation and progressive periodontitis forms at very tender age while in others, the rate of progression of the disease might take a lifetime (Kinane et al. 39). In such individuals the total loss of periodontal function is minimal. Some gingival sites also are more susceptible to the disease than others in the same mouth.

Detection of gingivitis is the most efficient method of screening for the disease (Kinane et al. 39). Self-detection could also be used which involves the observation of blood during brushing of teeth. Prevention of chronic periodontal diseases starts from controlling gingivitis. This can be done by preventing the formation of a microbial biofilm or regularly removing it at regular intervals. It can be done by maintaining a self-performed oral hygiene on a daily basis and further to that the professional removal of the biofilm on a bi-annual basis. However, recent studies have indicated that for low-risk patients who have few or even have no risk factors at all. Annual professional prophylaxis could be enough.

There are some known management practices that could be employed to treat or reduce the prevalence of this disease. They include non-surgical therapy which is the mechanical removal of both subgingival and super gingival dental plaque and root cleaning with local anesthesia. The overall outcomes depend on the skills of the operator and the skill and motivation of the patient in the cleaning of the teeth at home. To enhance the non-surgical treatment, some adjuncts in the form of medication that have been brought out. These adjuncts include drugs and systemic antibiotics (Kinane et al. 44). Drugs are delivered directly to the periodontal pockets in form of powder, gel or fire delivery system for localized treatment. Systemic antibiotics which are broad-spectrum antibiotics can be used alone or in combination with other antibiotics. No surgical therapy can be beneficial in controlling the disease (Kinane et al. 45). However, it still has some limitations this is in that there might be the need to control inflammation and optimize the outcomes

The second management technique is the use surgical therapy. The article describes that open debridement, a procedure in which a section of the gingiva is surgically separated from the underlying tissues. This is with the aim of providing access to the lesion (Kinane et al. 38). Reducing pocket surgery which involves the resection of soft and hard tissues using various techniques. Periodontal therapy has the potential to control the disease progression by ten-fold (Kinane et al. 39). The long-term success, however, depends on the cleanliness maintenance after active treatment has been completed.

Experimental gingivitis in man

The article shows that there is a very big relationship between oral deposits and the development and maintenance of periodontal disease (Löe et al. 23). It further shows that a relationship amongst periodontal damage and oral fragments exists. Biochemical and microbiological research suggests that an infection of the periodontal is an outcome of an interaction of the activities of bacteria and tissues of the host. Another experiment carried out and explained in this article indicates that a quantitative difference exists between inflamed gingivae as compared to microbial flora and healthy gingivae (Löe et al. 174). This article mainly deals with experiments aiming at showing the prevalence, amounts and possible causes of gingivitis in a human being. There is the conduction of experiments like micropsy and electron micropsy which tests and shows the relationship between the gingival tissues and microorganisms of the deposits. Another experiment is the clinical experiments which show that debris accumulation in the teeth leads to inflammation of the gingival. Other investigations show that when the debris is detached from the area, inflammation of the gingiva subsidizes. The main purpose or aim of this article is to show the experiments done on gingivitis in man.  In patients with health living gingivae, it attempts to produce gingivitis, by the withdrawal of oral cleanliness and hygiene maintenance efforts (Löe et al. 156). The article concludes that withdrawal of oral hygiene measures among the test individuals led to soft debris accumulation and gingivitis development. It further found that the time necessary for gingivitis to develop varies from ten to twenty-one days of complete withdrawal of oral hygiene (Löe et al. 134). The number of organisms in the gingivae increased with time. However, when oral hygiene was taken back, healthy gingival conditions were established once again.

Prevalence of periodontitis in adults in the United States: 2009 and 2010

In the United States of America in the year 2009 and 2010, a survey carried out concluded that of the individuals aged thirty years and above, incorporated in the survey, forty-seven percent of people in the United States had periodontitis (Eke et al. 916). These percentages were further divided to represent age groups. This is where those aged above sixty-five years were reported to have the disease more than other groups. This is evident in that seventy percent of the total periodontitis positive individuals were from this age bracket. Those between the ages of thirty to thirty-four added up to twenty-four percent.

It was also noted that periodontitis was higher in males than in females which would have been as a result of males continued habit of smoking (Eke et al. 917). Females tend to observe general body cleanliness and hygiene which most men do not, and this also happens in the oral hygiene. The disease was higher in Mexican Americas as compared to other racial and ethical groups (Eke et al. 916). People with low levels of education are most likely to get the disease as compared to those highly educated which results in higher incidences in high poverty levels. In general, the disease prevalence gets more severe with progressing age..

Microbiology of periodontal disease

Presently, micro-organisms are the primary etiology agents of this disease. This can be demonstrated by removal of debris in the mouth or removal of dental plaque by rigorous plaque control procedures. These procedures were first done by Loe and co-workers. These procedures which might also involve the use antiseptic agents could reverse or prevent the cases of clinical gingivitis in humans (Socransky 158). The destructive periodontitis could be completely or partially reversed by clinical procedures which involve surgical procedures but have to be followed by professional tooth cleaning twice a month by a dentist and proper oral hygiene observation. This can completely stop or even reverse the process of deterioration. Since it is now known that micro-organisms are the primary etiology agents of this disease, the question that many researchers remain to ask is which are the specific micro-organisms responsible?

The relationship between aggressive, destructive periodontal disease and gingivitis is still undergoing the re-evaluation (Socransky 157). Gingivitis might be defined as a response to the accumulated levels of micro-organisms but how it causes destructiveness is still unknown. According to Socransky (165) researchers came up with two hypotheses that tried to explain how this might occur. The first suggests that the disease activates the host’s immune pathological process which would lead to an acceleration of the condition leading to the destruction of tissues. The second argues that if the local bacteria component in the body is altered, either by addition of a new species of the pathogen or local overgrowth of the already present pathogen will lead to the initiation of tissue destruction.

For the destructive diseases, most of which are less encountered, there have to be some prerequisites to be met. If one of these conditions is not met, then the destructiveness of the disease will not be manifested. These conditions include; the number of pathogens which have to be at a significant number enough to initiate a disease, these organisms must be situated in a way that either the organism or the products from this organism must reach the target tissue, the host must also be susceptible (Socransky 163). The environment must allow the development of these pathogens, and there must be an absence of inhibitors either mechanical, biological or chemical inhibitors. Alteration of any of the five conditions for a disease to manifest itself will inhibit the initiation of the disease. This can be used as a method of completely stopping the disease

Other treatment ways should be introduced other than the mechanical debridement. These methods could include the use of microbial control of the disease. In this case, we will have to proceed in two distinct phases. Phase one involves targeting the pathogen, establishment of faster identification methods and optimal elimination methods. Phase two involves prevention which can be carried out by rapid removal of dental plaque (Socransky 159). Prevention could also be done by; suppressing the potential pathogens before the destructive disease is initiated, the establishment of host-compactible microbiota in individuals which would discourage the establishment of the potential pathogens and finally immunization programs.

 

The management of inflammation in the periodontal disease

As time goes, there is a better understanding of the causes and signs of periodontal disease. The article describes that there are a better understanding of the pathways of inflammation and the molecular basis of inflammation resolutions emerged. This is centered at the active and agonist-mediated return of tissues homeostasis. Anti-inflammation is interventions I inflammatory pathways while resolution biological pathways of restoring homeostasis (Van Dyke & Thomas, 165). The article reviews the resolution of inflammation in periodontal disease context and the potential for modification. Work In the animal models has the potential of therapeutic approach for treatment and intervention of the pathogenesis understanding of the human periodontal disease.

Theories of disease progression

Traditionally there were theories used to explain the progression of the disease. Among these theories is the theory that destructive periodontitis develops at a slow and consistent rate starting with the cumulative tissue loss to the complete loss of a tooth and the theory that there might be different periods of high-peak and lessening in the process of destruction (Bandyopadhyay et al 504). However, little evidence is available on whether one or both possibilities could occur in two individuals

Currently, the progression theory that is known is the intermittent theory. It is similar to the traditional as it indicates that there are periods of activity and periods of inactivity during the destruction progression of the disease. It further explains that the tissues destruction takes place sporadically which is accompanied by short periods of activity followed by inactivity periods which might take several months (Bandyopadhyay et al 507). The theory further explains that this tissue destruction occurs at different rates in different parts of the mouth. The theory also explains that susceptibility to the disease varies to a great extent from person to person and it is apparently determined by the host response to the periodontal pathogens

The studies conducted in these articles help in strengthening the theories of the disease progression. This is shown in that there are experiments that are conducted and shows that the progression of the disease is intermittent as the theories suggest. Still, there is the proving of the fact that the disease does not occur at all corners of the mouth at the same rate. The primer article shows images of the disease progression where some teeth develop the disease faster than other teeth. There is also the genetic representation and explanation, which shows that not all people are susceptible to the disease.

Age of the articles brings about a high percentage of variation. However, most of the research being carried out today is out of suggestions for further research made from previous articles. During the year 2009 and 2010, the percentage of children under the age of thirty were not commonly affected by the disease. In the recent, most children have adopted ways of living that resembles that of the adults. These ways of living have contributed to the increasing instances of aggressive periodontal disease among children (Bandyopadhyay et al 509). Some of the previously published articles conducted their research using different parts of the mouth. This leads to errors as periodontal diseases does not manifest itself evenly in all corners of the mouth. Recent research should include all corners of the mouth during their research.

Works Cited

P.I. Eke1, B.A. Dye2, L. Wei3, G.O. Thornton-Evans3, and R.J. Genco. “Prevalence of Periodontitis in Adults in the United States: 2009 and 2010.” Journal of Dental Research, vol. 91, no. 10, 2012, pp. 914-920.

Denis F. Kinane1, Panagiota G. Stathopoulou1 and Panos N. Papapanou “Periodontal diseases.” Nature Reviews Disease Primers, vol. 3, 2017, p. 17038, doi:10.1038/nrdp.2017.38.

Löe, H., Harald Löe,* D.D.S., Dr. Odont., Else Theilade, D.D.S. & S. B Örglum Jensen, …D.D.S., Lic. Odont.,  Aarhus, Denmark. “Experimental Gingivitis in Man.” Journal of Periodontology, vol. 36, no. 3, 1965, pp. 177-187, doi:10.1902/jop.1965.36.3.177.

Socransky, S. S. “Microbiology of Periodontal Disease—Present Status and Future Considerations.” Journal of Periodontology, vol. 48, no. 9, 1977, pp. 497-504.

Van Dyke, Thomas E. “Control of inflammation and periodontitis.” Periodontology 2000, vol. 45, no. 1, 2007, pp. 158-166.

Bandyopadhyay, Dipankar, et al. “Periodontal disease progression and glycaemic control among Gullah African Americans with type-2 diabetes.” Journal of Clinical Periodontology, vol. 37, no. 6, 2013, pp. 501-509.

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