The gingiva, or gum, is the keratinized oral mucosa covering the alveolar processes of the jaws, encircling the necks of erupted teeth (Figure 1).
Gingivitis, or inflammation of the gingiva, is the most common disease in dogs and cats. When left unrecognized and untreated, this inflammation can progress to tissue swelling, bleeding and periodontal disease.
Anatomically, the gingiva is divided into the marginal and attached areas.
Marginal gingiva. The free gingival margin passively lies against the tooth extending coronally from the free gingival groove. The inner surface (next to the tooth) of the free gingiva forms the gingival wall of the sulcus. The marginal gingiva extends from the free gingival margin to the attached gingiva (Figure 2).
Attached gingiva. The attached gingiva extends apically from the free gingiva to the alveolar mucosa. It is firmly bound to the underlying cementum and bone with collagen fibers of the connective tissue. Attached gingiva is keratinized to withstand the stress of mastication. The width of the attached gingiva varies in different areas of the mouth and is widest at the maxillary canines (Figures 3A and 3B).
The attached gingiva meets with the loose alveolar mucosa at the mucogingival junction, also referred as the mucogingival line. The mucogingival junction remains stationary throughout life, although the gingiva around it may change in height because of attachment loss.
Gingival epithelium is divided into three zones:
• The oral epithelium, also called the outer gingival epithelium, is a keratinized or para-keratinized covering of the oral surface of the attached gingiva and gingival papillae.
• The sulcular epithelium is the non-keratinized extension of the oral epithelium into the gingival sulcus. The gingival sulcus is a shallow space between the marginal gingiva and the tooth. The sulcus depth is generally under 1 mm but varies depending on the specific tooth and the size of the cat or dog (Figure 4).
• The junctional epithelium attaches to enamel of the most apical portion of the crown by means of hemidesmosomes and lies at the floor of the sulcus, immediately coronal to or at the cementoenamel junction. The junctional epithelium and gingival connective tissue separate the periodontal ligament from the oral environment. The floor of the gingival sulcus is located on the most coronal junctional epithelial cells.
Gingivitis. Gingivitis is the beginning stage of periodontal disease in which inflammation is confined to the gingival soft tissues only. This inflammation does not clinically extend into the alveolar bone, periodontal ligament or cementum. Periodontitis is the more established form of periodontal disease in which there is actual loss of the tooth-supporting tissues involving the periodontal ligament, alveolar bone and cementum.
Gingivitis can be present without periodontitis. Periodontal disease can exist without gingivitis in an area of previous periodontitis that has been treated and controlled, relieving inflammation but not attachment loss (Figures 5A and 5B).
Gingival bleeding. Bleeding on probing is indicative of an inflammatory process in the connective tissue adjacent to the junctional epithelium. If the sulcular lining is intact and healthy, no bleeding will occur. However, if periodontal disease is present, bleeding will usually occur. For localized and generalized bleeding on probing without loss of tooth support, local antibiotics such as clindamycin hydrochloride (Clindoral—TriLogic Pharma) can be injected into the pocket after cleaning to help reduce the bacterial load to help reduce the inflammation (Figures 6 and 7A-7C).
Gingival enlargement. Gingival hyperplasia and hypertrophy are histologic terms used to describe the clinical appearance of gingival enlargement, an increase in the size or thickness of the gingiva. Hyperplasia refers to an increased number of normal cells in a normal arrangement, and hypertrophy refers to an increase in the size of individual cells. Both of these conditions can only be accurately diagnosed microscopically. When viewed clinically without histologic confirmation, the condition is correctly called gingival enlargement.
There may be a genetic predisposition in boxers, rottweilers and Golden retrievers. Gingival hyperplasia may also occur secondary to medication administration, including cyclosporine and ACE inhibitors such as amlodipine (Figures 8A-8D).
Gingival recession. Gingival recession results in the exposure of the root surface by apical migration of the gingival margin. The periodontal attachment level (PAL) is an accurate measurement of periodontal destruction in cases of gingival recession where little or no pocketing exists. The PAL is measured from the base of the gingival sulcus/periodontal pocket to the cementoenamel junction. The clinical pocket depth plus recession (measured from the cementoenamel junction to the gingival margin) equals the total periodontal attachment loss (Figure 9).