Chapter 27. Gingival and Periodontal Infections

Gingivitis and periodontitis are inflammatory conditions of the tooth-supporting structures (periodontium). The transition from primary to permanent dentition, and the hormonal changes associated with puberty present unique periodontal conditions in children.1 In adults, these diseases are of a chronic nature, whereas in children they can be aggressive in nature. Thus, early diagnosis and treatment are critical. The nondestructive nature of gingival inflammation of childhood can progress to the more significant periodontal disease seen in the adult population if left untreated.1

Gingivitis and periodontitis are the two major forms of inflammatory diseases affecting the periodontium.2 Broadly speaking, gingivitis refers to reversible inflammation of the gingiva that does not result in clinical attachment loss. In contrast, periodontitis implies inflammation of both the gingiva and the adjacent attachment apparatus, and is characterized by loss of connective tissue attachment and alveolar bone. Each of these diseases may be further classified based upon etiology, clinical presentation, rate of progression, or associated complication factors as follows3,4:

• Dental plaque-induced gingival diseases
• Chronic periodontitis
• Aggressive periodontitis
• Periodontitis as a manifestation of systemic diseases
• Necrotizing periodontal diseases

Dental Plaque-Induced Gingival Disease

Dental plaque-induced gingival disease can be characterized by redness and edema of the gingival tissue, bleeding upon provocation, changes in contour and consistency, presence of calculus and/or plaque, without radiographic evidence of crestal bone loss (Figure 27–1).5

Chronic Periodontitis

Chronic periodontitis is more prevalent in adults, but can occur in children and adolescents. Chronic periodontitis is characterized by edema, erythema, gingival bleeding upon tissue manipulation, and suppuration with variable degrees of clinical attachment loss. In addition, radiographic evidence of bone loss and increased tooth mobility might be present.6 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).3 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.4

Aggressive Periodontitis

Aggressive periodontitis encompasses the distinct type of periodontitis that affect children, who, in most cases, appear healthy. Aggressive periodontitis can be presented in localized (LAgP) or generalized (GAgP) pattern. The localized version has a circumpubertal onset with familial aggregation, and there is a rapid rate of disease progression around first molars and incisors (Figure 27–2).7 However, atypical pattern of affected teeth are possible.7 Characteristically, the amounts of microbial deposits are inconsistent with the severity of periodontal tissue destruction.7 Thus, the primary features of localized aggressive periodontitis include a rapid clinical attachment and bone loss with familial aggregation.4 Secondary features include phagocyte abnormalities and a hyperresponsive macrophage phenotype.4 Generalized aggressive periodontitis is classically a disease of adolescent and young adults, but it can begin at any age. There is generalized interproximal attachment loss affecting at least three permanent teeth other than the first molars and incisors.7 Smoking may be a risk factor for this disease.

Systemic Causes of Periodontitis

Periodontitis as a manifestation of systemic disease in children is a rare disease that often begins between the time of eruption of the primary teeth (at about 6 months of age) up to the age of 5 years.8,9 Systemic etiologic components may be suspected in children who exhibit periodontal inflammation or destruction, which appears disproportionate to the local irritants.10 Conditions that make children more susceptible to periodontal disease include hematologic and genetic disorders (Table 27–1). 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.8,9 In the generalized form, there is rapid bone loss around nearly all teeth and marked gingival inflammation.8,9 In some forms of this disease, the primary and permanent dentitions can be affected. In addition, gingival enlargement or gingival overgrowth can be associated with drugs such as anticonvulsants (e.g., phenytoin), calcium channel blockers (e.g., nifedipine), and immunosuppressants (e.g., cyclosporin).

Necrotizing Periodontal Diseases

Necrotizing periodontal diseases are caused by abnormal overgrowth of normal oral bacteria as a consequence of poor oral hygiene.11 Necrotizing periodontal diseases manifest in two different forms: necrotizing ulcerative gingivitis and necrotizing ulcerative periodontitis.12 Necrotizing ulcerative gingivitis (also known as Trench mouth or Vincent's infection) is an acute infection of the gingiva, and when necrotizing ulcerative gingivitis has progressed to include attachment loss, it is known as necrotizing ulcerative periodontitis. The two most significant findings used in the diagnosis of necrotizing periodontal diseases are the presence of interproximal gingival tissue necrosis and ulceration, and the rapid onset of halitosis and gingival pain.4 Other findings often include lymphadenopathy, fever, and malaise.12

Specific Considerations and Presentations

Periodontal abscess is an acute suppurative infection of the deeper periodontal tissues that may lead to the destruction of periodontal ligament and alveolar bone.12 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; and/or increase in pocket depth.12 In addition, the tooth may be sensitive to percussion and may be mobile.12 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 administration of antibiotics.13

Linear gingival erythema is a manifestation of human immunodeficiency virus (HIV) infection. This condition is distinguished by 2–3 mm marginal band of intense erythema in the free gingiva, which may extend into the attached gingiva as a focal or diffuse erythema and extend beyond the mucogingival line into the alveolar mucosa.14 Treatments include improving oral hygiene, scaling and root planing, chlorhexidine rinses, and frequent dental cleaning.13

Inadequate brushing and flossing are by far the most common causes of gingivitis and periodontitis. Without proper brushing, plaque (a film-like substance made up primarily of bacteria) remains along the gum line of the teeth. Plaque also accumulates in faulty fillings and around the teeth next to poorly cleaned partial dentures, bridges, and orthodontic appliances. When plaque stays on the teeth for more than 72 hours, it hardens into tartar (calculus), which cannot be completely removed by brushing and flossing. Long-term accumulation of plaque and tartar leads to the creation of pockets between the teeth and gums. These pockets extend downward between the root of the tooth and the underlying bone, leading to destruction of the supporting bone and loosening of the tooth.

Dental plaque-induced gingival disease is compounded by bacterial accumulation that induces pathological changes in the tissues by direct (i.e., bacterial-derived byproducts) and indirect paths (i.e., host-derived inflammatory mediators). Although the microbiology of dental plaque has not been completely characterized, increased subgingival concentrations of Actinomyces spp., Capnocytophaga spp., Leptotrichia spp., and Selenomonas spp. have been found in experimental gingivitis in children when compared with gingivitis in adults.15,16 Histopathological observations have led to the subdivision into three stages that consist of vasodilation, increased gingival crevicular fluid, emigration of neutrophils, and activation of monocytes, lymphocytes, and fibroblasts.11 In addition, normal and abnormal fluctuation in hormone levels can modify the gingival inflammatory response to dental plaque, leading to a diagnosis of puberty or menopausal gingivitis.17,18

The pathology of chronic periodontitis lesions are characteristic of, and consistent with a subversion of host defenses against bacterial plaque pathogens and subsequent activation of bacterially induced host mediated processes that destroy periodontal tissues.11 The predominance of a gram-negative bacterial flora (Actinobacillus actinomycetemcomitans, Tannerella forsythensis, Porphyromonas gingivalis, Prevotella intermedia, and Fusobacterium nucleatum) in combination with the cellular and cytokine profiles of the lesions, indicate the likelihood that bacterial lipopolysaccharide activation of monocytes and subsequent production of tissue destructive cytokines is likely a major pathway for connective tissue attachment loss and bone loss.11

Highly virulent strains of A. actinomycetemcomitans in combination with Bacteriodes-like species are involved in localized aggressive periodontitis.19–21 In addition, a variety of functional defects have been reported in neutrophils from patients with LAgP.22,23 These include anomalies of chemotaxis, phogocytosis, bactericidal activity, superoxide production, FcγRIIIB (CD 16) expression, leukotriene B4 generation and Ca2+ channel, and second messenger activation.4 Even though the influence of these functional defects on the susceptibility of individuals to LAgP is unknown, it is possible that they play a role in the clinical course of disease in some patients.4 Generalized aggressive periodontitis is also frequently associated with periodontal pathogens A. actinomycetemcomitans and P. gingivalis, and neutrophils function abnormalities.4,7 For example, a poor serum antibody response to infecting agents is frequently detected.7 Smoking can increase the progression of periodontitis, and is sometimes an attribute to generalized aggressive periodontitis.

Neutrophils from some children with periodontitis as a manifestation of systemic disease have abnormalities in a cell surface glycoprotein (LFA-1 and Mac-1).4 Thus, the neutrophils in these patients having leukocyte adhesion deficiency are likely to have a decreased ability to move from the circulation to sites of inflammation and infection.24 In addition, affected sites harbor elevated percentages of putative periodontal pathogens, such as A. actinomycetemcomitans, P. intermedia,Eikenella corrodens, and Capnocytophage sputigena.25,26 Since there are several systemic diseases that cause periodontitis in young patients, health care providers need to be cognizant of all of possible hematologic and genetic disorders. In addition, health care providers need to determine appropriate clinical and laboratory tests that need to be performed in order to determine specific etiology of disease. Unfortunately, sometimes both the primary and permanent dentition can be lost due to underlying systemic conditions, such as Down syndrome and Papillon–Lefèvre syndrome, a rare autosomal recessive disorder characterized by palmoplantar keratoderma with periodontitis followed by premature shedding of both deciduous and permanent teeth (Table 27–1).

Necrotizing ulcerative periodontal disease sites harbor high levels of spirochetes and P. intermedia.27,28 The role of an impaired host response in necrotizing ulcerative gingivitis has long been recognized. For example, factors that predispose children to necrotizing periodontal disease include an altered immune system (response), viral infections, malnutrition, emotional stress, lack of sleep, and a variety of systemic diseases.29–31

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.6 In addition, appropriate supportive periodontal maintenance that includes personal and professional care is important in preventing reinitiation of inflammation.2 Since contributing systemic risk factors may affect treatment and therapeutic outcomes, elimination, alteration, or control of these risk factors should be attempted, and consultation with the patient's physician will likely be indicated to coordinate medical care in conjunction with periodontal therapy (Figure 27–3).6 For example, early nontraumatic tooth loss in children 3–18 years of age warrants evaluation for systemic causes of periodontitis.

Periodontal therapy will likely include patient education and hygiene.5 For gingivitis, rinsing several times a day with a hydrogen peroxide solution (3% hydrogen peroxide mixed with equal parts water) or chlorhexidine will reduce bacterial burden and hasten disease resolution. For periodontitis, debridement of tooth surfaces to remove supragingival and subgingival plaque and calculus is necessary. Unlike gingivitis, which usually resolves with improved oral hygiene, periodontitis requires professional care. A person using good oral hygiene can clean only 2–3 mm below the gum line. A dentist can clean pockets up to 4–6 mm deep using scaling and root planing which thoroughly remove tartar and the diseased root surface. In some cases (e.g., localized aggressive periodontitis), antibiotics, such as tetracycline in combination with scaling and root planing, are beneficial. Correction of ill-fitting restorations, caries, and tooth malposition will reduce the likelihood of plaque retention. Gingival deformities may require surgical correction using one of the following approaches6:

• Gingival augmentation therapy
• Regenerative therapy (i.e., bone replacement grafts, guided tissue regeneration, combined regenerative techniques)
• Resective therapy (i.e., flaps with or without osseous surgery, gingevectomy)

Long-term outcomes in children with periodontal diseases depend on patient compliance with treatment regimens and the delivery of professional periodontal maintenance at appropriate intervals.7 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. An appropriate initial interval for follow-up care and dental prophylaxis should be determined by the clinician; typically, a return visit occurs within 4–6 weeks.

If the patient is not better, there may be continuing clinical signs of disease progression with the possible development of periodontal defects. Factors that may contribute to the periodontal condition not resolving include lack of effectiveness and/or patient's noncompliance in controlling plaque, untreated underlying systemic disease, presence of calculus buildups, and patient's noncompliance with dental prophylaxis interval.

In the management of patients where the periodontal condition does not resolve, treatment may include additional sessions of oral hygiene instruction and education, additional or alternative methods or devices for plaque removal, medical/dental consultation, additional tooth debridement, increasing the frequency of dental prophylaxis, microbial assessment, and continuous monitoring and evaluation to determine further periodontal treatment needs.