Chapter 377. Periodontal and Gingival Health and Diseases

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. In children, similar characteristics are observed and recorded (although there are more spaces between primary teeth resulting in a “flatter,” less scalloped appearance). 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 If the conditions are left untreated, the deciduous or permanent dentitions can be jeopardized. Fundamental principles concerning the etiology of these diseases and the contributing factors need to be understood in order to identify and manage periodontal disease complications.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. 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). Systemically, patients with an impaired host response are at a higher risk to get periodontitis. AIDS, agranulocytosis, and neutropenia are examples of diseases that place patients at higher risk for periodontitis. Some young patients with localized aggressive periodontitis have depressed function of circulating polymorphonuclear leukocytes (PMNs) or monocytes.18 Ethnic and socioeconomic factors have also been associated with the incidence and prevalence of periodontitis.19 African American children have a higher prevalence of localized aggressive periodontitis than Caucasian children.20,21

The classification system for children and young adults has evolved over time. The most recent classification system has taken into account the latest information of pathophysiology, diagnosis, host defense, and microbiology.22 The five groups of gingival and periodontal diseases that occur most often in children and adolescents are listed below.22

Dental Plaque-Induced Gingival Diseases

Dental plaque-induced gingival diseases are the most prevalent forms of periodontal disease in children and adolescents and are typically caused by nonspecific bacterial infections.23

• Gingivitis associated with dental plaque only
• Gingival diseases modified by systemic factors
• Gingival disease modified by medications
• Gingival diseases modified by nutrition

Chronic Periodontitis

Chronic periodontitis in young people is much more prevalent than other forms of periodontitis. This is a nonaggressive disease featured by a more localized and less severe periodontal tissue loss. It is believed to be similar to chronic adult periodontitis.12 Local factors and environmental risk factors appear to play a major role in the initiation and progression of this disease, with a smaller role for genetic predisposition.12 Poor oral hygiene, local plaque-retaining factors, and smoking are important causative factors.

• Localized
• Generalized

Aggressive Periodontitis

Aggressive periodontitis is characterized by severe and rapid loss of periodontal tissues that commences at or after the circumpubertal age.12 These diseases are caused by multiple factors, and there is a significant genetic predisposition. Local factors appear to play a considerable role in the etiopathogenesis of these diseases. Aggressive periodontitis is more frequent in older age groups and in certain ethnic groups, particularly those of African or Hispanic descent.12

• Localized
• Generalized

Periodontitis as a Manifestation of Systemic Diseases

Periodontitis as a manifestation of certain systemic diseases usually commences before puberty and may affect the deciduous and permanent teeth.12 These diseases have a clear genetic etiology, although local factors may be responsible for initiating the periodontal inflammation.12

Associated with Hematological Disorders

• Acquired neutropenia
• Leukemias
• Other

Associated with Genetic Disorders

• Familial and cyclic neutropenia
• Down syndrome
• Leukocyte adhesion deficiency syndromes
• Papillon-Lefèvre syndrome
• Chediak-Higashi syndrome
• Histiocytosis syndrome
• Glycogen storage disease
• Infantile genetic agranulocytosis
• Cohen syndrome
• Ehlers-Danlos syndrome (types IV and VII)
• Hypophosphatasia
• Other
• Not otherwise specified (NOS)

Necrotizing Periodontal Diseases

Necrotizing periodontal diseases are associated with a diminished host resistance to bacterial infection of periodontal tissues, and this immunosuppression may occur due to various environmental factors such as malnutrition, psychological and physical stress, poor oral hygiene, alcohol use, and smoking.12 Necrotizing periodontal diseases are more common in the poor populations of underdeveloped countries.

• Necrotizing ulcerative gingivitis (NUG)
• Necrotizing ulcerative periodontitis (NUP)

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.24

However, 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 lipopolysaccharide 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.51-54 Microbiological 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

Histologically, ulceration of the sulcular epithelium and inflammatory cell infiltration of the underlying connective tissue characterize gingivitis.25 Periodontitis are destructive forms of periodontal diseases that are characterized by inflammation of the periodontal tissue, leading to an apical migration of the epithelial attachment and loss of periodontal soft and hard tissues.26

The genetic component of periodontal disease can impact the initiation, path of progression, and response to treatment.27,28 The genetic components responsible for the development of the extracellular matrix of the periodontium may play a part in some forms of periodontitis.29-31 The genetic regulation of the host defense system can also affect the progression of periodontitis.32 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 In addition, one study that examined 117 pairs of adult twins revealed that, after adjusting for dental care and smoking, the risk for chronic periodontitis was approximately 50% heritable.34 Other data suggests that genetic factors may play a greater role in the pathogenesis of periodontal tissue loss in the aggressive forms of periodontitis.35 Recent studies have revealed that aggressive periodontitis is inherited as an autosomal recessive or autosomal dominant disease.12 In addition, it has long been recognized that severe attachment loss often accompanies certain genetic disorders such as the Papillon-Lefèvre syndrome, Down syndrome, congenital neutropenia, leukocyte adhesion deficiency, Chediak-Higashi syndrome, and other heritable syndromes.12

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).1 Mild 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

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 Both the localized and generalized forms of aggressive periodontitis show a rapid progression of disease, and in the absence of early detection and treatment, the affected teeth usually show increased mobility due to the severe loss of supporting tissue and may eventually be lost.

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 Both primary and permanent dentitions can be affected. 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).

Necrotizing Periodontal Disease

Necrotizing periodontal diseases are caused by abnormal overgrowth of normal oral bacteria as a consequence of poor oral hygiene.59 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 Severe cases may show the presence of a pseudomembrane, swelling of lymph nodes, fever, and malaise.13 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

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. In eliciting this pertinent information, the child or adolescent’s parents or guardians may be a reliable source of information.1 Clinically, 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 In addition, appropriate supportive periodontal maintenance that includes personal and professional care is important in preventing a recurrence of inflammation.68 Since contributing systemic risk factors may affect treatment and therapeutic outcomes, elimination, alteration, or control of these risk factors should be attempted, and consultation between the patient’s pediatrician and the dentist is usually indicated to coordinate medical care with periodontal therapy.48 Specific treatment for periodontal disease is determined by the patient’s age, overall health, medical history, and extent of the disease.

The clinical findings together with a diagnosis and prognosis should be used to develop a logical treatment plan in order to eliminate or alleviate the signs and symptoms of periodontal diseases and thereby arrest or slow further disease progression.67 A broad range of therapies exist in periodontics, and no single treatment approach can provide the only means of treating any one or all periodontal diseases.67 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 expectorate.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 Examples of surgical therapies are resective therapy (ie, flaps with or without osseous surgery, gingivectomy), regenerative therapy (ie, bone replacement grafts, guided tissue regeneration, combined regenerative techniques), and gingival augmentation therapy.

For example, 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. The interval between the maintenance therapy visits depends on the patient’s response to treatment, plaque control, and the initial diagnosis.1 Recall intervals of no more than 4 months are appropriate for most patients who have been successfully treated.

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

In patients for whom the periodontal condition does not resolve, treatment might include additional sessions of oral hygiene instruction and education, additional or alternative methods or devices for plaque removal, medical/dental consultations, additional tooth debridement, increased frequency of dental prophylaxis, microbial assessment, and continuous monitoring and evaluation to determine further periodontal treatment needs.67 Informed consent should always be obtained prior to commencing therapy.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