ETIOLOGY/PATHOPHYSIOLOGY

The gingiva covers the alveolar processes of the mandible and maxillae and conforms closely to the neck of the tooth
The gingiva is divided into attached and free, or marginal, portions: the attached gingiva is tightly bound to the periosteum overlying the alveolar processes; the marginal gingiva extends above the crest of the alveolar bone and tapers to a knifelike edge that lies in contact with surface of the tooth
The gingival sulcus: the narrow cleft between the inner wall of the marginal gingiva and the tooth; in dogs, normally <2–3 mm but may be deeper around the canine teeth in large-breed dogs; in cats, normally <1 mm
The junction between the gingiva and buccal oral mucosa appears as a distinct line or furrow called the mucogingival line or junction
The connective tissue of the gingiva (lamina propria) contains an extensive array of blood vessels, lymphatics, nerves, and collagen fibers; plasma cells, lymphocytes, and neutrophils are also abundant and are important in local defense mechanisms
Crevicular fluid (gingival crevicular fluid [GCF]): plasma-derived; passes from the gingival connective tissue through the crevicular epithelium to lavage the gingival sulcus; flow occurs in response to bacteria (plaque) in the gingival sulcus; contains immunoglobulins, other nonspecific antibacterial substances, and neutrophils as the predominant cells; important in controlling the bacterial population
In healthy animals, gram-positive aerobic cocci and rods predominate in supragingival plaque; anaerobes are more abundant subgingivally, and spirochetes are found tightly packed in the apical region of the gingival sulcus
As gingivitis develops, anaerobes and spirochetes become increasingly more abundant in the subgingival sulcus
In dogs, the bacteroides organisms (Bacteroides, Prevotella, Porphyromonas spp.) and Fusobacterium spp. appear to be important pathogens; Porphyromonas and Peptostreptococcus spp. are common in samples from cats with gingivitis
Gram-negative organisms: increase in number as gingivitis develops; invade tissues and elaborate endotoxins that can result in tissue destruction
The fact that these bacteria are present in disease and health and that periodontal disease does not progress in linear fashion (i.e., periods of active disease are followed by quiescent periods) indicates that host–bacteria interaction is important in the pathogenesis of periodontal disease
Plaque: composed of bacteria, polymorphonuclear neutrophil leukocytes (PMNs), and salivary glycoproteins; forms within 24 hours on clean tooth surfaces; the gingiva’s inflammatory response to plaque consists of vasculitis, edema, and collagen loss
Gingivitis of different severity can exist in one patient’s mouth, based on the host’s immunocompetency and local oral factors
- Gingivitis is also referred to as stage 1 periodontal disease (see Chapter 26)
- Early gingivitis: a small amount of plaque, mild gum line erythema, and smooth gingival surfaces (Figs. 25-1 and 25-2)
- Advanced gingivitis: subgingival plaque and calculus, moderate to severe erythema, and irregular gingival surfaces
Risk factors
- Age
- Head shape and occlusive pattern; crowding of teeth reduces natural cleaning mechanisms (toy and brachycephalic breeds)
- Toy breeds affected earlier in life
- Soft foods
- Open-mouth breathing
- Chewing habits
- Lack of oral health care
- Metabolic diseases such as uremia and diabetes mellitus predispose to more pathogenic oral bacteria
- Autoimmune diseases such as pemphigus vulgaris and systemic lupus erythematosus