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While gingival crevicular fluid provides for the cellular defence and humoral factors to combat against the microbial insult, the gingival crevicular fluid also deliver novel substrates, in the form of proteins and glycoproteins, for bacterial metabolism. These include haeme containing molecules and iron, such as haemoglobin and transferrin.
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.
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.
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]
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.
The gingival tissue forms a crevice surrounding the tooth, similar to a miniature, fluid-filled moat, wherein food debris, endogenous and exogenous cells, and chemicals float. The depth of this crevice, known as a sulcus , is in a constant state of flux due to microbial invasion and subsequent immune response.
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]
The EA is very strong in a healthy state, acting as a type of seal between the soft gingival tissue and the hard tooth surface. The deepest layer of the JE, or basal layer, undergoes constant and rapid cell division, or mitosis. This process allows a constant coronal migration as the cells die and are shed into the gingival sulcus.