Gingival inflammation usually is caused by accumulation of bacterial plaque at the adjacent tooth surface. This plaque may be seen in histologic sections as a deep blue mass lying at the surface of the tooth. Toxins of these bacteria as well as enzymes from the attracted neutrophils cause damage to the junctional epithelium that loses its fixation to the tooth. In this way, a niche is created between gingiva and tooth in which further plaque accumulation may occur. The thin layer of junctional epithelium becomes spongiotic and hyperplastic and may even disappear resulting in ulceration. Also, elongated rete ridges develop that penetrate into the underlying fibrous tissue forming the bulk of the free gingiva. In this connective tissue, an inflammatory infiltrate evolves that may be either acute, subacute or chronic (Fig. 9.1a, b). In due time, the inflammation involves the underlying periodontal bone that will be resorbed, thus causing loss of the fixation of the tooth in the jaw bone. At this stage, gingivitis has evolved into periodontitis that will be discussed in section “Periodontitis”.

Gingival hyperplasia may be generalised in which case one speaks of gingival fibromatosis (Fig. 9.2). It may also occur confined to a limited area of the jaw, then it is called an epulis fibrosa (Fig. 9.3