Nadeem Y. Karimbux and David M. Kim
The normal periodontium consists of gingiva, connective tissue, the periodontal ligament, cementum, and the surrounding alveolar bone. Clinicians commonly describe the healthy gingiva as being scalloped, coral pink in color, firm, and knife-edged. The lack of bleeding on probing and the lack of exudates are also taken as clinical signs of health. There are several different forms of gingival and periodontal diseases that can be present in children and adolescents that can change the appearance (erythematous), contour (swollen), size (hyperplastic or overgrown), and shape (blunted papillae) of the gingiva. They range from reversible conditions limited to the inflammation of gingival tissues (gingivitis) to those characterized by the destruction of the periodontal connective tissue attachment and alveolar bone (periodontitis).1
According to the American Academy of Periodontology, periodontal disease in children and adolescents can be classified into five distinct periodontal disease categories (eTables 377.1 and 377.2 )2:
1. Dental plaque-induced gingival diseases
2. Chronic periodontitis
3. Aggressive periodontitis
4. Periodontitis as a manifestation of systemic diseases
5. Necrotizing periodontal diseases
EPIDEMIOLOGY
Even though epidemiological studies indicate that gingivitis of varying severity is nearly universal in children and adolescents, these studies also indicate that the prevalence of destructive forms of periodontal disease is lower in young individuals than in adults.2 The reported prevalence of periodontitis in children and young adults varies by age. Children ages 5 to 11 years have a reported prevalence rate of up to 9%; those ages 12 to 15 years have a prevalence rate up to 46%.3-10 Thus, children and adolescents should receive a periodic periodontal evaluation as a component of routine dental visits, because periodontitis is usually preceded by gingivitis.
A national survey showed that gingivitis that is found in early childhood is more prevalent and severe in adolescence and then tends to become less severe in older age groups.11 Chronic periodontitis in children and adolescents is more common than the other three forms of periodontitis listed above, and it is clinically similar to the chronic periodontitis seen in adults.12 The prevalence of aggressive periodontitis varies significantly between various demographic groups.13 Periodontitis as a manifestation of systemic diseases and necrotizing periodontal diseases occur more often in children than in adults, though both are relatively uncommon.14,15
Periodontitis is a multifactorial disease, and there are several local and systemic factors that are associated with it. For example, local contributing factors such as caries, inadequate restoration, and subgingival calculus may contribute to a bacterial accumulation that will result in a host-mediated inflammatory response16,17 (eFig. 377.1 ). Ethnic and socioeconomic factors have also been associated with the incidence and prevalence of periodontitis.19African American children have a higher prevalence of localized aggressive periodontitis than Caucasian children.20,21 Patients with various disorders are at increased risk for peridontitis that usually manifests before puberty. Most of these disorders are due to genetic defects that likely alter local factors, initiating the periodontal inflammation.12 These include diabetes mellitus, neutropenias and neutrophil disorders, leukemias, Down syndrome, Papillon-Lefèvre syndrome, Chediak-Higashi syndrome, histiocytosis syndrome, glycogen storage disease, Ehlers-Danlos syndrome (types IV and VII), and hypophosphatasia.1 Systemic diseases such as measles and impaired endocrine balance, in combination with malnutrition, can also render the host susceptible to the onset of these diseases.12
PATHOPHYSIOLOGY
Bacterial accumulation that results in a cascade of host-mediated inflammatory response is the pathway of periodontal soft and hard tissue destruction. Aggregatibacter actinomycetemcomitans, Prevotella intermedia, Porphyromonas gingivalis, Tannerella forsythensis, and Treponema denticola are gram-negative organisms that have been found in children and young adults with periodontal attachment loss.24However, only a subgroup of microorganisms might be responsible for the initiation of the tissue destruction in chronic periodontitis.46,47 The predominance of a gram-negative bacterial flora (Aggregatibacter actinomycetemcomitans, Tannerella forsythensis, Porphyromonas gingivalis, Prevotella intermedia, and Fusobacterium nucleatum) in combination with the cellular and cytokine profiles of the lesions indicates the likelihood that bacterial lipopolysaccha-ride activation of monocytes and subsequent production of tissue-destructive cytokines is likely to be a major pathway of destruction.48
Results of several studies suggest that Aggregatibacter actinomycetemcomitans is a major etiologic factor in the pathogenesis of aggressive periodontitis.49,50 Functional abnormalities in neutrophils and monocytes taken from localized aggressive periodontitis patients have been reported, such as increased adherence, abnormal signal transduction, depressed chemotaxis, and other related functions.51-54Microbiological and histological studies in patients with necrotizing periodontal disease have shown the presence of spirochetes, gram-positive cocci, β-hemolytic streptococci, Borrelia species, P gingivalis, P intermedia, and Candida albicans.63
The genetic component of periodontal disease can impact the initiation, path of progression, and response to treatment.27,28 A study in twins estimated that 38% to 82% of the population variance in clinical measures of periodontal diseases might be attributable to genetic factors.33
CLINICAL MANIFESTATIONS
Dental Plaque-Induced Gingival Diseases
Typical features of gingivitis may include gingival redness, swelling, marginal bleeding, and pseudopockets in the absence of bone loss, which might be reversible following appropriate therapy (Fig. 377-1).1Mild and moderate forms of gingival inflammation are an almost universal finding in young people.3,38 Normal and abnormal fluctuation in hormone levels, including changes in gonadotrophic hormone levels during the onset of puberty, can enhance the gingival inflammatory response to dental plaque.43,44
FIGURE 377-1. Clinical evidence of dental plaque-induced gingival disease, especially on lower anterior teeth.
Chronic Periodontitis
Chronic periodontitis can be classified based on disease severity and extent of involvement. Disease severity can be categorized into mild (1–2 mm clinical attachment loss), moderate (3–4 mm clinical attachment loss), or severe (≥ 5 mm clinical attachment loss).22 In addition, the disease can be localized (less than 30% of the dentition affected) or generalized (greater than 30% of the dentition affected) and is characterized by a slow to moderate rate of progression that may include periods of rapid destruction.2
The key features of chronic periodontitis are apical migration of junctional epithelium, loss of periodontal connective tissue attachment, alveolar bone loss, and pocket formation.1 Studies of the role microorganisms play in the pathogenesis of chronic periodontitis concluded that the amount of bacteria and bacterial products that accumulate locally in the periodontal tissue is of prime importance resulting in attachment loss (Fig. 377-2).45
Aggressive Periodontitis
Aggressive periodontitis can be subdivided into localized or generalized forms based on the extent, severity, and type of teeth affected.13 Localized aggressive periodontitis is characterized by severe periodontal tissue loss at the first molars and incisors and an age of onset between the circumpubertal age and late adolescence.13 Generalized aggressive periodontitis is also characterized by a rapid and severe periodontal tissue loss at the first molars and incisors, although the disease is not limited to these teeth and involves more than three other teeth.13
Periodontitis as a Manifestation of Systemic Diseases
This category of periodontitis can occur in localized and generalized forms. In the localized form, affected sites exhibit rapid bone loss and minimal gingival inflammation.55,56 In the generalized form, there is a rapid bone loss around nearly all teeth and marked gingival inflammation.55,56 Gingival enlargement or gingival overgrowth can be associated with drugs such as anticonvulsants (eg, phenytoin), calcium channel blockers (eg, nifedipine), and immunosuppressants (eg, cyclosporin), more or less related to the dosage and the amount of plaque buildup. As noted above, a variety of systemic diseases, particularly those that impact neutrophil function, place individuals at increased risk of periodontal disease (see Epidemiology section above).
FIGURE 377-2. Clinical evidence of childhood chronic periodontitis, especially of upper posterior molars.
Necrotizing Periodontal Disease
These periodontal diseases manifest in two forms: necrotizing ulcerative gingivitis (NUG) and necrotizing ulcerative periodontitis (NUP).60 NUG is a distinctive periodontal condition characterized by a rapid onset of intense gingival pain, spontaneous bleeding, necrotic ulceration of the gingival tissue, a fetid odor, and destruction and necrosis of one or more interdental papillae.13,61,62 If untreated, the disease may lead to loss of periodontal tissue and may develop into necrotizing ulcerative periodontitis.13 NUP may be a sequel of a single or recurrent episode of NUG, or it may occur as a result of necrotizing disease at a site previously affected by perichondritis.13 The differential diagnosis for NUG includes primary herpetic gingivostomatitis, caused by primary contact to herpes simplex virus type 1.1
PERIODONTAL ABSCESS
Periodontal abscess is an acute suppurative infection of the deeper periodontal tissues that may lead to the destruction of periodontal ligaments and alveolar bone (Fig. 377-3).64 Patients may complain of localized pain and swelling with progression over hours or days, heat sensitivity, fever, and gingival bleeding. Clinical features may include a smooth, shiny swelling of the gingiva; pain, with the area of swelling tender to touch; a purulent exudate; or increase in pocket depth.64 In addition, the tooth may be sensitive to percussion and may be mobile.64 More severe infections lead to trismus, dysphagia, respiratory difficulty, face or neck swelling, and regional lymph node involvement. Treatments include irrigation and mechanical debridement of the pocket, drainage and debridement of the lesion, and antibiotics.65
FIGURE 377-3. Clinical evidence of periodontal abscess on mandibular incisor areas.
LINEAR GINGIVAL ERYTHEMA
Linear gingival erythema is a manifestation of HIV infection. This condition is distinguished by a 2 to 3 mm marginal band of intense erythema in the free gingiva, which may extend into the attached gingiva as a focal or diffuse erythema and may extend beyond the mucogingival line into the alveolar mucosa.66 Treatments include improving oral hygiene, scaling and root planing, chlorhexidine rinses, and frequent dental cleaning.65
DIAGNOSTIC EVALUATION
A definitive diagnosis requires a detailed medical and dental examination. The dental assessment includes a clinical examination, periodontal charting, and dental radiographs. If on examination the pediatrician observes heavy plaque and calculus accumulation as well as edema, redness, bleeding, recession of the gingiva, or tooth mobility, referral for further evaluation is indicated (Fig. 377-4). Microbiological, genetic, biochemical, or other diagnostic tests may also be useful, on an individual basis, for assessing the periodontal status of selected patients or sites.67
TREATMENT
In general, the therapeutic goals of periodontal treatment are to alter or eliminate the microbial etiology and contributing risk factors for periodontal disease, thereby arresting the progression of disease and preserving the dentition.48
FIGURE 377-4. Presence of heavy plaque buildups and clinical signs of inflammation would require consultation with a dentist.
Periodontal treatment should be completed in three phases: initial therapy, surgical corrective therapy, and maintenance therapy.1 Initial therapy includes patient education to eliminate or control plaque accumulation and the debridement of tooth surfaces to remove supragingival and subgingival plaque and calculus deposits.1 Toothbrushing twice daily with fluoridated toothpaste is recommended. A power toothbrush may be efficacious if the patient is unable to brush effectively. Although certain mouthwashes containing various pharmaceutical agents (3% hydrogen peroxide mixed with equal parts water or 0.12% chlorhexidine) have some adjunctive antiplaque effect in adults, mouthwashes are not generally indicated in young children due to their inability to expecto-rate.1 Antibiotic treatments, such as doxycycline, metronidazole, or metronidazole/amoxicillin combination, may be utilized in the initial therapy. For example, in the treatment of localized aggressive periodontitis, tetracycline administration with scaling and root planing has been shown to be effective. Surgical corrective therapy might be indicated to provide access for plaque removal and to restore function and aesthetics.48
Gingival overgrowth (gingival hyperplasia) should initially be treated by improved plaque control, scaling, and adjunctive antibacterial mouthwash. If the patient does not respond to these initial treatments, one can employ surgical treatment options such as gingivectomy or flaps with or without osseous surgery to eliminate the hyperplastic tissue (eFig. 377.2 ). Maintenance therapy is performed to prevent disease recurrence and progression and includes follow-up care.
COMPLICATIONS
The results of periodontal treatment may be adversely affected by circumstances beyond the dentist’s control. Examples of such circumstances include systemic diseases; inadequate plaque control by the patient; unknown or undeterminable etiologic factors that current therapy has not controlled; pulpal-periodontal problems; inability or failure of the patient to follow the suggested treatment or maintenance program; adverse health factors such as smoking, stress, and occlusal dysfunction; and uncorrectable anatomical, structural, or iatrogenic factors.67
A satisfactory response to therapy should result in a significant reduction in clinical signs of gingival inflammation, stability of clinical attachment levels, and reduction of clinically detectable plaque to a level compatible with gingival health. Long-term outcomes in children with periodontal diseases depend on patient compliance with treatment regimens and the delivery of professional periodontal maintenance care at appropriate intervals.69