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It is caused by precipitation of minerals from saliva and gingival crevicular fluid (GCF) in plaque on the teeth. This process of precipitation kills the bacterial cells within dental plaque, but the rough and hardened surface that is formed provides an ideal surface for further plaque formation.
These include defence cells and proteins such as Neutrophils, Antibodies and Complement, and various plasma protein. With the outflow of the Gingival Crevicular Fluid (GCF) into the gingival sulcus, at a rate of approximately 0.2ul per hour, that significantly increases with the presence of periodontal disease, this produces a “washing effect ...
In addition to acting as a buffer, saliva and gingival crevicular fluid contain primary nutrients including amino acids, proteins and glycoproteins. This feeds the bacteria involved in plaque formation. The host diet plays only a minor role in providing nutrients for the resident microflora. [21]
The early lesion displays acute exudative inflammation; exudative components and crevicular lymphocytes reach their maximum levels between days 6–12 after plaque accumulates and gingival inflammation commences [21] with the quantity of crevicular fluid being proportional to the size of the reaction site within the underlying connective tissue.
They migrate from the tissues in a specialized exudate called gingival crevicular fluid also known as GCF. Neutrophils are recruited to the gingival crevice area as they are signalled to by molecules released by plaque microorganisms. Damage to epithelial cells releases cytokines which attract leukocytes to assist with the inflammatory response.
Probing should be avoided then, and an analysis by gingival index should determine the presence or absence of inflammation. The monthly reevaluation of periodontal therapy should involve periodontal charting as a better indication of the success of treatment, and to see if other courses of treatment can be identified.
Oral Microbiology Lab Analysis Report. [10] The oral microbiome, mainly comprising bacteria which have developed resistance to the human immune system, has been known to impact the host for its own benefit, as seen with dental cavities. The environment present in the human mouth allows the growth of characteristic microorganisms found there.
Tobacco smoking impairs phagocytic and chemotactic activities of leukocytes [17] and impedes wound healing, [18] specifically by affecting gingival blood flow. [19] [20] Cigarette smokers are more likely to experience destruction of the alveolar bone and periodontal ligament and are at a higher risk of developing periodontal disease. [21] [22]