Redness and edema, usually without pain (Fig. 6.1).
• Gingival hyperplasia may sometimes be observed (Fig. 6.2).
• Bleeding may occur spontaneously, or after light probing.
• There is often halitosis.
• The diagnosis is made clinically.
Differential diagnosis
• Desquamative gingivitis
• Drug-induced gingival hyperplasia
• Gingivitis due to mouth breathing
• Acute leukemia
Treatment
• Plaque control and good oral hygiene.
• Gingivectomy, in cases of severe gingival hyperplasia.
Periodontitis
Definition
• Periodontitis is the result of progression of the inflammatory process from the gingiva to the deeper periodontal structures.
Etiology
• Bacterial plaque is important for the initiation of the disease.
• The same factors as in chronic gingivitis, which usually evolve into periodontitis.
• Systemic predisposing factors include: diabetes mellitus, human immunodeficiency virus (HIV) infection, immune diseases, metabolic diseases, etc.
• Host factors are also important, and appear to be influenced by genetic and environmental factors such as smoking.
Occurrence in children
• Rare, mainly in adolescents.
Localization
• Localized or generalized.
Clinical features
• The consequences of periodontitis are alveolar bone resorption and loss of attachment, followed by periodontal pocket formation.
• Inflammation and edema of the gingiva, pockets deeper than 3 mm (Fig. 6.3).
• Bleeding and malodorous breath, teeth migration, tooth movement.
• The diagnosis is usually made clinically.
Radiographic features
• Alveolar bone resorption.
Differential diagnosis
• Papillon–Lefèvre syndrome
• Langerhans’ cell histiocytosis
• Acatalasia
• Hypophosphatasia
• Leukemia
• Glycogen storage disease Type Ib
• Scurvy
Treatment
• Plaque control and good oral hygiene.
• Scaling and root planing and/or surgery.
• Maintenance therapy is very important.
Fig. 6.1 Chronic gingivitis
Fig. 6.2 Chronic hyperplastic gingivitis
Fig. 6.3 Periodontitis
Juvenile Periodontitis
Definition
• Juvenile periodontitis is a specific type of early-onset periodontitis, which usually affects adolescents, and is characterized by severe alveolar bone loss.
Etiology
• Actinobacillus actinomycetemcomitans and probably other pathogens may be involved.
• Reduced immune response to endotoxins of bacterial plaque or genetic immune insufficiency have been proposed.
Occurrence in children
• Only in adolescents.
• Familial occurrence.
Localization
• Affects only permanent teeth.
• Localized or generalized.
• Selectively affects incisors and first molars.
Clinical features
• Mild gingival inflammation (Fig. 6.4).
• Rapid and severe destruction of alveolar bone.
• Deep periodontal pockets, bleeding, malodorous breath.
• Absence of local factors (bacterial plaque, calculus).
• Tooth mobility and migration (Fig. 6.5).
Radiographic features
• Severe and rapid bone loss (Fig. 6.6).
Differential diagnosis
• Prepubertal periodontitis
• Adult periodontitis
• Papillon–Lefèvre syndrome
• Ehlers–Danlos syndrome, type VIII
• Crohn’s disease
• Chediak–Higashi syndrome
• Ulcerative necrotizing periodontitis in HIV infection
