Inflammation of the gingiva - gingivitis - is caused by accumulation of dental plaque on the teeth. In the absence of adequate tooth-cleaning, plaque is formed at the gingival margin and on approximal surfaces. In these locations, the contours of the teeth and gingiva facilitate the retention of salivary microorganisms. Gradually, the plaque increases in thickness and extends over the tooth surfaces. Plaque left undisturbed at the gingival margin will cause an inflammatory reaction of the gingiva already within 3-4 days. The degree of inflammation will increase, and after 1-2 weeks, gingivitis can be observed at clinical examination (Fig. 22a, 22b, p. 28).
Gingivitis is reversible, that is, it may disappear and the gingiva may become healthy again, provided the teeth are cleaned and subsequently kept free from plaque. Most cases of gingivitis will heal within 1-2 months. Untreated gingivitis and continuous penetration of the plaque subgingivally may lead to injury to the supporting structures of the teeth (periodontal ligament, cementum and alveolar bone). Periodontitis may develop.
In gingivitis, changes take place both in the epithelium and in the connective tissue (Fig. 23a-23d, pp. 30-31). Inflammatory cells accumulate in the connective tissue, initially adjacent to the gingival sulcus. Polymorphonuclear leukocytes are found close to the epithelium. Lymphocytes and plasma cells predominate in the deeper layers of the connective tissue. The polymorphonuclear leukocytes migrate towards the microbial deposits. As they migrate, they may engulf isolated bacteria that have penetrated into the epithelium or into the connective tissue (phagocytosis). Lymphocytes and plasma cells are activated by microbial products (antigens) and result in the production ' of antibodies and other immune components. Monocytes, capable of developing into macrophages, also participate in the inflammatory reaction.
The collagen fibers in the connective tissue gradually disintegrate. Tissue fluids accumulate in the connective tissue (edema). The gingiva becomes clinically edematous (swollen) and the stippling on the surface may disappear. There is an increase in the number of patent blood vessels and their diameters widen. The permeability of the vessels also increases, allowing more serum and inflammatory cells (exudate) to pass through the vascular walls and accumulate in the tissue.
The sulcular epthelium and the coronal part of the junctional epithelium show both proliferative and degenerative changes. Epithelial rete pegs are formed and penetrate into the connective tissue. Thinning of the epithelium takes place, sometimes to the extent that ulceration may develop and expose the connective tissue directly to the subgingival microbial deposits.
Within the epithelium bordering the subgingival plaque, inflammatory cells, particularly polymorphonuclear leukocytes, are seen. The migration of these cells is facilitated by the widening of the junctions between the epithelial cells induced by the inflammatory reaction.
The plaque continues t6 penetrate subgingivally, and the inflammation gradually extends apically. The depth of the tissue changes is related to the degree of apical plaque penetration (Fig. 23a-23d, pp. 30-31; Fig. 24, p. 32).
Vascular changes
The vascular changes in gingivitis include altered vascular topography, increased vascular permeability and increased vascular fragility.
The course of the blood vessels changes and the number of vessels increases: vascular proliferation. The diameter of the vessels also increases. The network of vessels in gingival health, forming the dentogingival plexus, is transformed into a system with abundant vascular loops (Fig. 23a-23d, pp. 30-31; Fig. 25, p. 33).
The increase of vascular permeability leads to accumulation of fluids and inflammatory cells in the tissues and to exudation of fluids and cells into the gingival sulcus.
Vascular walls rupture more easily, resulting in easily elicited bleeding. Bleeding on toothbrushing is a useful warning signal, informing the patient that inflammation may be present. In cases of more severe gingivitis, spontaneous bleeding may also occur. The tendency to bleed in gingivitis is explained by increased fragility of vessels located more superficially beneath thinned areas of the sulcular and junctional epithelia.
End of Lecture