periodontal disease

Progression of periodontal disease

Many people would be so worried and would rush to a physician if they happened to wash their hands and started bleeding. But most people, however, clean their teeth, and starts bleeding but do not put much consideration to it. This is because it is almost normal to have a bleeding gum, while other people take it to be an injury from the toothbrush they use. This might not always be the case. It could also be an infection or a disease that would lead to more severe losses in future. Periodontal disease or gum disease as most people refer to it is an inflammation of the gum. It is a wide range of conditions related to the inflammatory effects that affect the supporting structures of teeth (Reynolds, Harmony & Ronald, 2016). These structures are the gingiva, bone, and periodontal ligaments. Inflammation of these structures can lead to complete loss of one tooth or many teeth in case the disease has affected a large portion of the gum. I can also lead to systemic inflammation. 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. Chronic incidences of the disease are evident in the adults while aggressive periodontitis may also affect children or adolescents (Reynolds et al., 2016).

The disease manifests itself in three stages from the least severe to the most severe. These stages are gingivitis, periodontitis, and advanced (Ganzetti, Giulia, Anna, Andrea, Valentina & Annamaria, 2014).

Oral hygiene is one of the predisposing factors for this disease. People who maintain a high oral hygiene are less likely to be infected by the disease. This is following increasing evidence from different research on dental fields which indicate that deposits in the mouth contribute a large percentage to the development and maintenance of the disease as well. However, there exist other factors that increase the risk of one contacting the disease. These factors might be controllable while others cannot be controlled. Examples of the controllable factors are smoking and tobacco use. It is believed that the use of tobacco and smoking increases the risk of periodontal 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, smoking accelerates it, and it becomes more severe. Stress is another factor that increases the risk. When a person is stressed, the body immune system weakens which in turn makes it hard for the body to fight the disease (Genco, Robert & Wenche, 2013). The decision to smoke or get stressed lies within an individual’s hands hence making the two to be controllable factors.

Some factors are not controllable. Some people are naturally susceptible to the disease because of their genetic composition. However, these people can escape from the disease to an extent by maintaining a good oral health. Misaligned or crowded teeth are another factor as it makes it hard for teeth cleaning process. People having this kind of a problem can contact the dentist closest to them for advice on the appropriate teeth cleaning ways. Fluctuating hormonal levels in the body during puberty or pregnancy can lead to changes in the mouth too which would lead to temporary risk (Socransky, 2013).

Understanding the signs associated with periodontal disease is important. This is because the disease can manifest itself, and the signs are sometimes painless (“Periodontal Disease: Causes and Prevention,” 2017). The known signs are examples of swollen, red, tender or bleeding gums, loose teeth, and persistent bad odor from the mouth and gums that move away from the tooth.

Traditionally there were theories that were 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. Another theory stated that there might be different periods of high-peak and lessening in the process of destruction. However, little evidence is available on whether one or both possibilities could occur in two individuals (Charlene, 2012).

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. It is accompanied by short periods of activity which are accompanied by inactivity periods which might take several months. As a result, the whole process of destruction takes a long period before the actual falling off of the tooth. The theory further explains that this tissue destruction occurs at different rates in different parts of the mouth. Destruction does not occur in all corners of the mouth at the same time. Destruction only occurs with only specific tooth surfaces which greatly depend on the type of tooth and the level of hygiene. 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.

In the United States of America in the year 2009 and 2010, a survey was carried out to determine the prevalence of the disease which used data from the National Health and Nutrition Examination Survey. The survey concluded that of the individuals aged thirty years and above who were incorporated in the survey, forty-seven percent which represents more than sixty-four million people in the United States had periodontitis which was dispersed as; mild 8.7 percent, moderate 30 percent and 8.5 percent for severe periodontitis. 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 (Khan, Shahrukh, Khalid & Awan, 2016).

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. Females tend to observe general body cleanliness and hygiene which most men do not, and this also happens in the oral hygiene. As a result from this, males have higher incidences of the disease as compared to females. The disease was higher in Mexican Americas as compared to other racial and ethical groups (Bandyopadhyay, Dipankar, Nicole, Jyotika & Renata, 2010). 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 (Khan et al., 2016).

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 (Charlene, 2012). These procedures which might also involve the use antiseptic agents could reverse or prevent the cases of clinical gingivitis in humans. 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 (Socransky, 2013).

This can completely stop or even 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 (Charlene, 2012)?  Many laboratories are continuing with the examination of the micro-organisms. However, these experiments have been experiencing a lot of problems concerning technical difficulties. There have been reported cases that different forms of periodontal disease might have specific microbial etiologies (Shakibaie, Fardad, Laurence & Walsh, 2016).

The relationship between aggressive, destructive periodontal disease and gingivitis is still undergoing the re-evaluation. Gingivitis might be defined as a response to the accumulated levels of micro-organisms but how it causes destructiveness is still unknown, and it is an open area of more research. However, 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 (Socransky, 2013).

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. If nothing reaches the target tissue, no matter how many organisms are available, no disease will be initiated. The host must also be susceptible to illness and the organisms causing the disease. The environment in which these pathogens fall on must allow the development and reproduction of these pathogens, in other words, the environment must be conducive and lastly, there must be an absence of inhibitors either mechanical, biological or chemical inhibitors (Socransky, 2013).

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. For instance, if the number of pathogens is reduced or the distance between the pathogen and the target tissue increased, then the disease will not be initiated. In case this is maintained for a long period then it means that the disease will be eliminated. The same would happen if there were microbial inhibitors in the target tissue (Socransky, 2013).

In the treatment of this disease, other treatment ways should be introduced other than the mechanical debridement which is the continuous removal of dental plaque. 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. 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 (Socransky, 2013).

Contrary to the previous percentage of forty-seven in the year 2009 and 2010, as of September 2012, findings from the Centre for Disease Control and Prevention (CDC) of the United States indicated that in Chicago alone, fifty percent or one out of every two individuals have periodontal disease. This is a significant increase which reflects that soon almost seventy percent of people will have this disease. The type of food and legalization of smoking in most states are some of the predisposing factors to the rise in this disease (Shakibaie et al., 2016).

The articles provided shows that there is a very big similarity between them and the present findings of the disease. This is evident in some theories like the one explaining the progression of the disease as an intermittent process. However, there are some notable differences in the two, for instance, it states that the only method of prevention is the removal of the dental plaque while in the present, and there are other ways for prevention which include the microbial methods.

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 (Shakibaie et al., 2016).  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.

Periodontal disease or the gum disease should be taken with much weight as it may lead to more severe infections these infections could result in using a lot of funds to treat or even cause death. Periodontal disease is associated with other conditions like diabetes (Bandyopadhyay et al., 2010), heart disease and plaque and tartar. People also should regularly visit their dentists to check for any signs of periodontal disease. Some controllable causes of periodontal disease should be avoid smoking and stress are only but a few examples of these causes. Proper nutrition, diseases screening, and prevention minimized the use of medicine and observing the general hygiene in the mouth are other examples of the measures that should be taken to minimize periodontal disease incidences. Avoid clenching of teeth to live healthy, have fresh breath and appealing gum.

Works Cited

Shakibaie, Fardad, and Laurence J. Walsh. “Dental calculus detection using the VistaCam.” Clinical and Experimental Dental Research 2.3 (2016): 226-229. Print.

Socransky, S. S. “Microbiology of Periodontal Disease—Present Status and Future Considerations.” Journal of Periodontology 48.9 (2013): 497-504. Print.

Charlene W.J. “The Microbial Aetiology of Periodontal Diseases.” Periodontal Diseases – A Clinician’s Guide (2012): n. pag. Print.

Ganzetti, Giulia, Anna Campanati, Andrea Santarelli, Valentina Pozzi, and Annamaria Offidani. “Periodontal Disease: An Oral Manifestation of Psoriasis or an Occasional Finding?” Drug Development Research 75 (2014): S46-S49. Print.

Khan, Shahrukh, Taimur Khalid, and Kamran Awan. “Chronic periodontitis and smoking. Prevalence and dose-response relationship.” Saudi Medical Journal 37.8 (2016): 889-894. Print.

Reynolds, Harmony R., and Ronald G. Craig. “Atherosclerotic Vascular Disease and Periodontal Disease.” A Clinician’s Guide to Systemic Effects of Periodontal Diseases (2016): 39-51. Print.

Genco, Robert J., and Wenche S. Borgnakke. “Risk factors for periodontal disease.” Periodontology 2000 62.1 (2013): 59-94. Print.

“Periodontal Disease: Causes and Prevention.” Oral Health and Dental Care | Colgate® Oral Care. N.p., n.d. Web. 28 Sept. 2017.

Bandyopadhyay, Dipankar, Nicole M. Marlow, Jyotika K. Fernandes, and Renata S. Leite. “Periodontal disease progression and glycemic control among Gullah African Americans with type-2 diabetes.” Journal of Clinical Periodontology 37.6 (2010): 501-509. Print.

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