Postulate of Periodontal Disease The pervasiveness of periodontitis has evolved over the past forty to fifty years. During the 1950s and 1960s, the disease has begun to surface in the teenage years until the early middle age where almost every adult has been afflicted. Today, it’s quite different. Results from a survey in the mid-1980s from the National Institute of Dental Research reveal that moderate to severe periodontitis affect individuals between the ages of eighteen and sixty-five.
However, in the United States alone, tens of millions of individuals are affected while hundreds of millions of individuals are affected all across the world. Periodontitis, ultimately, continues to be a dominant health problem in the United States and all around the world. People came to the conclusion in the mid-1980s that the pervasiveness of periodontitis is not common, which drove clinicians and investigators to start looking at the disease in terms of risk and to diagnose aspects that separate the people and groups who are vulnerable to periodontitis from those who are not.
As much as bacteria play their role in the disease, the host factors play a larger role in the pathogenesis; therefore articulation of host factors is a new and advantageous way to prevention and treatment. In the forefront of the early 1980s, the formation of periodontal pockets was equal to having periodontitis and it has been told that once it starts and if not treated immediately, it will progress incessantly until tooth loss ensued. This creed was overturned by a study Lindhe et al. operated in 1982.
A group of individuals with fairly severe periodontitis was tested before and were watched over for six years. After the six years are up, they found that the condition of periodontitis in those patients had about 11 percent of teeth worsen and most of the dissolving sections were detected in small divisions of the patients. These examinations were accepted and reached to other groups with advanced periodontitis, to societies in other countries and to groups that were previously treated.
All of these led to the same result: the presence of periodontal pockets is not equal to active periodontitis. It is clear that both active and inactive pockets exist and that most periodontal pockets and periodontal degradation in patients are not disease-active and are digressive and sporadic; however, for a small amount of patients about 3 percent to 5 percent, the disease advancement is persistent and swift which will not react fairly to any form of remedy. The knowledge gained from these results has a considerable impact on day-to-day practice.
For the most part, periodontal diseases are infective. In the oral cavity alone, there are 300 species, serotypes, and ribotypes of bacteria as well as a dozen species are involved in the origin of periodontitis in humans. Experts decided that the species, Porphyromonas gingivalis, Bacteroides forsythus, and Actinobacillus actinomyceteomitans, all gram-negative and anaerobic, are responsible for most cases of periodontitis. Periodontitis is a disease caused by a small group of primarily anaerobic gramnegative bacteria that create biofilms on the tooth surfaces.
The elease toxic materials like lipopolysaccharide as well as develop low molecular weight metabolites. These toxic materials have precisely destructive effects on the barrier epithelium and can inject themselves into the connective tissues, come into contact with small vessels and cells of the host, to activate an inflammatory feedback. At that point, millions of phagocytic neutrophils make a voyage to the sulcus, to cover the biofilms. Eventually, distinguished antibodies are created and they cooperate with the phagocytic neutrophils.
The host’s defenses are of no use and the immuneinflammatory reaction leads to tissue destruction. But before periodontitis forms, it becomes gingivitis first. Gingivitis is the feedback to microbial plaque and the marginal and interdental gingiva become severely inflamed and bulky. The disease’s development is completely regressed by tooth cleaning and superb daily oral hygiene; nonetheless, in vulnerable patients with treatment and without treatment, the disease will advance to periodontitis.
In advanced periodontitis, the gingival tissues appear bulky and inflamed while the disease in prolonged periodontitis, the gingival tissues become fibrotic and the teeth become loose and spread apart due to the bone loss and deep periodontal pockets. Newly cleaned teeth are immediately covered up by pellicles that are made up of glycoprotein from saliva. The gram-positive bacteria from saliva touch upon adhesions that carefully bind to pellicle and settle colonization and growth of supragingival plaque.
Not long after, the gramnegative species migrate through particular receptor binding to the gram-positive bacteria. If left freely, deeply adherent microbial plaque becomes visible on the tooth surface at the gingival margin and an intense inflammatory reaction develops. In patients vulnerable to the buildup of periodontitis, bacteria spread into the gingival sulcus and create subgingival plaques that are closely holding on to the tooth surface. Those plaques resemble characteristics of biofilms.
Biofilms are labeled as “matrix-enclosed bacterial populations adherent to each other and/or to surfaces or interfaces. “(1) Experts observed and have found proof that the bacteria broadcast with each other and shape formations with a fundamental circulatory system. Biofilms enclose diverse microenvironments that differ in pH, oxygen tension, and possibilities of specific nutrients. It’s crucial to understand the biofilms perception to grasp the pathobiology of periodontitis and its association to efficient diseases.
In circumstances of biofilms, subgingival plaques are stubbornly persistent and a pain to eliminate. Gingival fluids contain complement, antibodies, and all systems that exist in the blood to help avert and regulate infection. They progress into the periodontal pocket moderately submerging the biofilms. Activating the complement may happen, in which millions of leukocytes, and neutrophils in particular, unite at the biofilms surface. Still, bacteria thrive in the biofilms due to being protected from antibiotics and anti-bacterial drugs.
Gramnegative bacteria in biofilms emit vesicles that are abundant in lipopolysaccharides (LPS). The biofilms distribute a steady, restorative supply of lipopolysaccharide. When the epithelium pocket appears, it has entry to connective tissues and circulation. Substantial interruption and elimination are efficient ways of treating biofilms. For this reason, scaling and root planning are crucial in all prosperous forms of periodontal therapy.
Periodontitis is a clan of similar diseases. The American Academy of Periodontology observes several forms. These include localized and generalized prepubertal and juvenile forms, rapidly progressive, necrotizing ulcerative, adult, and refractory periodontitis. They vary in “etiology, natural history, disease progression, and response to therapy but they share common pathways of tissue destruction. ” (1) The common occasions in pathobiology are determined by disease alternates, or “risk factors and indicators” (1) in hereditary and indirect, in which they may vary from one phase and create disease to another.
The altered factors are the main elements of variety seen in various periodontal settings. They may affect age of disease onset, patterns of observed bone and tissue destruction, rates of disease progression, response to various kinds of therapy, and severity and frequency of disease recurrence. ” (1) These alternates may withstand for life while others including stress and smoking may be now or never, or differ in degree at different times in life; the harshness and amount of advancement of disease retaliation to impact the disposition and consequence of microbial threat by impacting pH and vacancy of oxygen and different nutrients in the periodontal pocket.
This admittance to pathobiology of periodontitis allows us to fully understand why people differ greatly in disease awareness, clinical displays, estimates of growth, and therapeutic acceptance. It grants knowledge to the relationship between oral health and general systematic health. The everyday defenses of the gingival sulcus are “low levels of plaque, low-level antigenic stimulation, junctional epithelium expresses IL-8 and ICAM-1, few venules express E-selectin and ICAN-1, and low-levels of PMN emigration into sulcus. (1)
In general noninflamed and mildly inflamed gingiva, a small number of venules in the connective tissue intended E-selectin and intercellular attachment molecule-1, better known as ICAM-1, and there is a recurring journey of leukocytes and in particular neutrophils, from the plexus in the blood vessels close to the epithelium-connective-tissue fuse over the top of the microbial plaque. The bacteria pursue a gradient of chemoattractant molecules containing Interleukin-8, made by the epithelial cells and peptides of the FMLP class discharged as metabolic products by the bacteria.
The bacteria’s journey is aided by the epithelial cells. They assemble on the top of the biofilms and generally restrict its lateral and apical extension. Major events of gingivitis are “microbial plaque that is better organized and more gram-negative enters sulcus, small gingival pocket with pocket epithelium forms, more venules become activated; enhanced expression IL-8, ICAN-1, E-selectin; enhanced PMN migration, enlarging infiltrate with B and T cells, plasma cells, macrophages, and PMNs are prominent. (1)
Because the gingival sulcus is invaded by biofilms and interrupts the union of the coronal chunk of the junctional epithelium and the tooth, the junctional epithelium changes the pocket epithelium into a gingival pocket, meaning the biofilms and its bacteria has easy access to the connective tissues and blood vessels. When this happens, the vessels of the microcirculation are more likely to be inflamed and passable. In conclusion, periodontal diseases are a serious health problem around the world.
From years of observations and experiments, we’ve learned that the disease progresses between the age of eighteen and sixty five, the presence of periodontal pockets are not a sign of active periodontitis and those three gram-negative, anaerobic species of bacteria are responsible for periodontitis. It is stated that each person has either a strong resistant or a weak resistant to periodontitis, which is why maintaining regular teeth cleaning and oral hygiene is important in keeping periodontitis from progressing.
