Abstract Gingivitis is caused by substances derived from microbial plaque accumulating at or near the gingival sulcus; all other suspected local and systemic etiologic factors either enhance plaque accumulation or retention, or enhance the susceptibility of the gingival tissue to microbial attack. Microbial species specifically associated with gingival health include Streptococcus sanguis1, 5. D‐7, and Fusobacterium naviforme. Bacteria involved in the etiology of gingivitis include specific species of Streptoccous, Fusobacterium, Aclinomyces, VeiUonella, and Treponema and possibly Bacteroides, Capnocytophaga, and Eikenella. Microbial colonization and participation is sequential, with the complexity of the associated flora increasing with time. The pathogenesis has been separated into the initial, early, and established stages, each with characteristic features. The initial lesion is an acute inflammation which can be induced experimentally by application of extracts of plaque bacteria to normal gingiva. The early lesion is characterized by a lymphoid cell infiltrate predominated by T lymphocytes, characteristic of lesions seen at sites of cell‐mediated hypersensitivity reactions. The early lesion can be induced by application of purified contact antigens to the gingival tissues of previously sensitized animals. As the clinical condition worsens, the established lesion appears, predominated by B lymphocytes and plasma cells. Established lesions may remain stable for indefinite periods of time, they may revert, or they may progress. Periodontal destruction does not result from the conversion of a predominantly T cell to a predominantly B cell lesion as has been suggested, but rather from episodes of acute inflammation. Clinical manifestations of gingivitis are episodic phenomena characterized by discontinuous bursts of acute inflammation. Most lesions are transient or persistent but not progressive. Attachment loss may precede alveolar bone loss and may occur without the manifestations of a concurrent or a precursor gingivitis. On the other hand, the evidence indicates that a portion of gingivitis lesions can and does progress to periodontitis. Gingivitis and the periodontal microflora differ in children and adults. Clinical signs of gingivitis either do not appear as plaque accumulates, or they are greatly delayed in children, and the inflammatory infiltrate consists mostly of T lymphocytes. The conversion to a B cell lesion does not appear to occur. The evidence supports the conclusion that gingivitis is a disease, and that control and prevention is a worthwhile goal and a health benefit. Efforts to achieve this goal should be continued and intensified, since we are as yet unable to distinguish between gingivitis lesions which will progress and those which will not.