Aggressive Periodontitis Paper

     Periodontal disease is more commonly known as gum disease or gingivitis. This infection is serious enough, that it can lead to tooth loss if left untreated. This chronic infection starts around the tooth and it affects the supporting bone and gums. Periodontal disease can affect anywhere from one tooth to all thirty-two teeth. The disease pathology starts with the plaque that builds up on your teeth everyday.

Skurska, A., Dolinska, E., Pietruska, M., Pietruski, J. K., Dymicka, V., Kemona, H., Arweiler, N. B., Milewski, R., Sculean, A. (2015). Effect of nonsurgical periodontal treatment in conjunction with either systemic administration of amoxicillin and metronidazole or additional photodynamic therapy on the concentration of matrix metalloprotrinases 8 and 9 in gingival crevicular fluid in patient 's with aggressive periodontitis. BMC Oral Health. doi: 10.1186/s12903-015-0048-0

Research shows that periodontitis might be connected with the development of cardiovascular disease. One theory is that the inflammatory proteins and the microorganisms in the periodontal tissue enter the circulatory system and cause different consequences for the cardiovascular system. Researchers know that inflammation leads to hardened arteries, called atherosclerosis. That is a condition that

Chronic periodontitis has been identified as the most prevalent form of periodontitis affecting the adults and occasionally the adolescents and children.(Merin, 2015) This periodontal disease of inflammatory origin is thought to be the result of host immune response against bacterial colonies in the subgingival plaque.(Merin, 2015) In many cases, systemic and environmental factors play a significant role in the disease progression. Common risk factors such as uncontrolled diabetes mellitus and smoking, contribute to periodontal destruction in genetically susceptible individuals by modifying the host’s immune reactions towards periodontal pathogens. Clinically, the diagnosis of chronic periodontitis is made based on the presence of supragingival and subgingival plaque and calculus, signs of gingival inflammation, periodontal attachment loss and radiographic bone loss. Chronic periodontitis can be further classified based on the extent and severity of periodontal destruction. Localised chronic periodontitis is diagnosed when less than 30% of the sites are affected; whereas the generalised form of the disease affects more than 30% of the sites. The severity of the disease is determined by the amount of clinical attachment loss. It is classified as mild, moderate or severe when 1-2mm, 3-4mm or 5mm or more attachment loss is recorded respectively. (Merin, 2015)

According to paper published by Eke, Wei, Thornton-Evans, and Genco in 2012, about 47% of the sample representing 64.7 million adults aged 30 yr and older had periodontitis. Not only that, adults aged 65yr and older had higher percentage

Periodontal disease is typically asymptomatic (not showing any signs) until the advanced stages. The most common factors of periodontal disease are genetic and environmental. Other factors that may

Apical periodontitis occurring after Root Canal Treatment presents a more complex etiologic & therapeutic situation than Primary Apical Periodontitis. There is a universal consensus that intra-radicular infection is an essential cause of primary as well as a major contributor of post treatment apical periodontitis. Enterococcus faecalis is the most commonly implicated microorganism in asymptomatic persistent infections1,2.

Gum disease (or periodontal disease) is an inflammation of tooth-supporting tissues. It is due to the accumulation of bacteria (referred to as plaque) at the junction between the teeth and gums.

(178) published a paper in the form of a clinical trial in order to examine the effect of periodontal treatment on the biological and clinical parameters of RA. Their proposed study was randomized controlled trial including participants with both RA and periodontitis. The investigators plan to involve a total of 40 individuals into two groups (intervention group including full-mouth SRP, followed by systemic antibiotics, amoxicillin or clindamycin, if allergic to penicillin, for seven days, oral hygiene instructions, and rinsing with 0.12 % chlorhexidine gluconate for 10 days after periodontal treatment). Patients will be followed for three months, and the same intervention will then be applied to the control group. The primary outcome of this study was a change in DAS28 score by decreasing RA activity. A major drawback of this study is the use of amoxicillin or clindamycin adjunctive to SRP. This antimicrobial approach should not be used as periodontal pathogens have been shown to be resistant to these

The long-term treatment plan for managing chronic periodontitis should include periodic monitoring of periodontal status and appropriate maintenance procedures.28 Experimental studies have reported very successful treatment outcomes when patients are professionally maintained at two-week intervals,161 but such a program is impractical for most chronic periodontitis patients. Therefore, to maximize successful therapeutic outcomes, patients must maintain effective daily plaque control. It also appears that in-office periodontal maintenance at three to four month intervals can be effective in maintaining most

Gingivitis and periodontitis are among the most common infectious diseases in human beings which results in bone loss, tooth loosening and eventually tooth loss. Although periodontopathic bacteria are the primary etiological agents in periodontal disease, the ultimate determinant of disease progression and clinical outcome is the host's immune response(1). Lymphocyte blastogenesis studies of peripheral blood from patients with periodontal disease also suggested the involvement of cell-mediated immunity(2). The inflammatory response in children is different from that of adults. The most prevalent type of gingival disease in childhood is chronic marginal gingivitis which is characterized by an infiltrate consisting mostly of T lymphocytes and

This essay will begin with a brief overview on chronic periodontitis to better facilitate the proper selection of abutment in patients with a history of the disease. Chronic periodontitis is a slowly progressive inflammatory disease that results in the destruction of periodontium, characterised by clinical attachment and alveolar bone loss (Armitage and Cullinan, 2010, Shaddox and Walker, 2010). For a patient with a history of chronic periodontitis,

Based on our clinical findings and the patient’s complaint, I believe the patient has symptomatic apical periodontitis. The likely anatomical structures affected are the pulp of #31 (needing root canal therapy), the periodontium surrounding #31, possible involvement of the gingiva surrounding #30 (tooth directly anterior to #31). Depending on the path the infection has taken, it could have caused bone resorption and the infection could be cause nerve pain if allowed to progress. Infectious material courses through the path of least resistance, so it likely would have traveled from the apex of #31 into the surrounding gingiva, and up through the sulcus. The infection could also spread into the vestibule or floor of the mouth causing swelling

There are many categories of periodontal disease. They include chronic periodontitis, aggressive periodontitis, disease-related periodontitis, and acute necrotizing periodontal disease. Just because you have gingivitis does not mean you will get periodontitis, in fact some experts believe that they are two very different diseases. Chronic periodontitis is basically the same thing as gingivitis but it has a few more symptoms including; halitosis, a persistent metallic taste in the mouth, and gingival recession. Most patients who have this will not even worry or they might not even know. Most of the time inflammation and bone destruction is painless, patients just assume that they just need to floss more or brush more often. This can often be solved by better oral care. Patients who suffer from aggressive periodontitis are normally younger than patients who have the chronic form. People who have this are generally healthy other than the presence of periodontal disease. These people will experience rapid loss of periodontal attachment fibers and bone destruction. They also will have a depressed neutrophil function, the neutrophils can also be defective, resulting in depressed chemotaxis and phagocytosis. Patients with this

Periodontitis is a chronic inflammatory disease process which is initiated by bacterial challenge and characterized by destruction of tooth supporting tissues. It is the most prevalent form of bone disease in humans and a modifying factor of systemic health of patients 1. However recent evidence suggests that mere presence of putative periodontal pathogens is not sufficient for initiation of disease process 2. It is rather persistent host inflammatory response against those pathogens that leads to periodontal tissue destruction 2.