Gingival and Periodontal Diseases in Children

Periodontal Diseases in Children

Periodontal diseases are significant health issues affecting both children and adults. In children, gingivitis is more prevalent than periodontitis. Bone and attachment loss are uncommon in children but can occur due to systemic diseases or isolated dental conditions. Early diagnosis and treatment are crucial for preventing future complications.

Introduction

Periodontal diseases in adults often begin in childhood, highlighting the importance of early dental intervention. Untreated periodontal diseases can negatively impact a child's nutrition and development. Periodontal tissues differ significantly between children and adults.

Periodontium in Primary Dentition

In primary dentition, gums have distinct characteristics compared to adult gums:

• They are typically pale pink.
• The attached gingiva is less keratinized, making underlying veins more visible.
• Stippling patterns appear around age 3 and are seen in about 56% of children aged 3-10 years.
• No significant differences between maxillary and mandibular arches or between genders have been reported during childhood.

Differences Between Periodontal Structures in Children and Adults

Key differences in periodontal structures between children and adults:

• Interdental Gingiva: Wide in the buccolingual direction but narrow in the mesiodistal direction. Papillae are flattened in interproximal areas, consistent with primary dentition morphology.
• Gingiva Consistency: Softer with a thick, roll-shaped margin. Appears more red during teething.
• Probing Pocket Depth: Shallower in primary teeth (approximately 1-2 mm), increasing in depth posteriorly.
• Attached Gingiva Width: Greater on the vestibule surfaces of anterior teeth compared to posterior teeth; narrowing may occur in the canine region. On lingual surfaces, width increases from anterior to posterior. Gingival width increases with age during the transition to permanent dentition.
• Junctional Epithelium: Thicker in primary teeth, reducing bacterial and toxin passage.

Characteristics of Periodontal Tissues in Childhood (Radiographically)

Radiographic features of periodontal tissues in children:

• The lamina dura is more prominent.
• The periodontal ligament space is wider.
• The periodontal membrane is thicker with less dense and more loosely arranged fibers.
• Cementum is thinner and less calcified.
• Alveolar bone is thinner with wider marrow spaces.
• Calcification is less, and there are more lymph and blood vessels.
• The alveolar crest is flatter, located 1-2 mm from the enamel-cementum boundary.
• Alveolar bone contains more organic matter.

Epidemiology

In developed countries, the incidence of gingivitis in children aged 6-11 is approximately 73%, increasing with age. Adolescence sees a significant rise in gingivitis prevalence, ranging from 50-99%. Gingivitis is reportedly less prevalent in girls, likely due to better oral hygiene.

Classification of Periodontal Diseases in Children and Adolescents

The American Academy of Periodontology classifies periodontal diseases in children and adolescents as follows:

1. Gingival Diseases
   • Gingival diseases induced by dental plaque
   • Gingival diseases not induced by dental plaque
2. Aggressive periodontitis
3. Chronic periodontitis
4. Periodontitis as a manifestation of systemic diseases
5. Necrotizing periodontal diseases

Gingival Diseases

Gingival Diseases Due to Dental Plaque

Plaque-induced chronic gingivitis is the most common periodontal infection among children and adolescents, with a reported incidence of 70% in children after age seven. Initial signs include swelling, bleeding, and redness in the marginal gingiva. Although progression to periodontitis is rare, treatment is essential. Dental plaque from poor oral hygiene is the primary cause.

Factors Affecting Gingivitis in Children

• Plaque and Gingival Index: No strong correlation exists between dental plaque scores and gingival index in children. Similar oral hygiene conditions result in milder disease development compared to adults.
• Dietary Habits: Differences in dietary habits.
• Dentition: Mixed dentition.
• Oral Hygiene: Incorrect and uncontrolled oral hygiene practices.
• Malocclusion: The presence of malocclusion.

The severity of gingivitis in children is generally milder than in adults due to:

• Differences in dental plaque composition.
• Variations in the immune system.
• Differences in periodontal structures.

Children's dental plaque contains fewer periodontal pathogens. Decreased vascularity and a thicker epithelial barrier limit the severity of infections. Gingivitis prevalence increases with age, peaking in puberty (ages 14-16) due to hormonal factors.

Clinical Features of Gingivitis

• Inflammation is typically limited to the marginal gingiva.
• Changes occur in gum color, size, and consistency.
• Progression starts with redness, swelling, and bleeding, potentially leading to chronic changes like fibrotic tissue and hyperplasia.
• In the absence of severe gingival hypertrophy or hyperplasia, there is no significant increase in pocket depth and bleeding.
• Histological evaluation shows cellular inflammatory cells infiltrating the junctional epithelium and collagen loss.

Inflammatory reactions are more pronounced in adults with similar plaque levels. Children exhibit a predominance of T lymphocytes and fewer B lymphocytes and plasma cells, resulting in a different host response. The thicker junctional epithelial barrier in children reduces permeability, making it more difficult for bacterial toxins to induce inflammation.

Eruption Gingivitis

Gingival inflammation during tooth eruption, resulting from increased plaque accumulation in areas where primary teeth are falling out and permanent teeth are erupting. These areas are sensitive, making hygiene maintenance difficult. Degenerative changes occur in the junctional epithelium during eruption, increasing the epithelium's permeability. Sulcus development is incomplete, and the gingival margin is not keratinized. Inflammatory changes alter the gingiva's normal form, leading to gingival enlargement.

Food entrapment may exacerbate the condition, potentially causing pericoronal abscess or pericoronitis. Effective plaque control can reduce these reactions.

Puberty Gingivitis

Several factors, including plaque scores, dental caries, tooth eruption, crowding, and mouth breathing, influence the severity and incidence of gingivitis in adolescents. However, the most significant factor is the surge in steroid hormones between ages 9-14, coinciding with pre-pubertal and pubertal periods. This increase has a temporary effect on the gums and resolves after adolescence.

Gums contain receptors with a high affinity for estrogen and progesterone. These are located in the basal layer of the epithelium, spinous layer, connective tissue endothelium, and fibroblast cells in small vessels. Hormones increase vascular permeability, potentially damaging the endothelium and affecting leukocyte migration, subgingival flora incorporation, and granulation tissue formation.

Inflammation increases earlier (ages 10-13) in girls due to increased hormone levels. Estrogen and progesterone levels are associated with higher P. intermedius rates, which uses these hormones as a food source.

Pubertal gingivitis is characterized by marked inflammation, bluish-red discoloration, edema, gingival enlargement, and spontaneous bleeding, particularly in interdental areas. Effective oral hygiene, elimination of local factors, and professional prophylaxis are very effective.

Gingival Growths Due to Drug Use

Gingival enlargement can occur due to the use of cyclosporine, calcium channel blockers, and phenytoin, with a high prevalence in children. Clinical and microscopic features are similar across different drugs. Growth begins in the interdental space and spreads to cover the marginal gingiva, potentially covering incisal and occlusal surfaces in severe cases. Enlargement is common throughout the mouth, especially in the maxillary and mandibular anterior regions. It is typically seen around teeth and disappears after extraction. Mucosal hyperplasia in edentulous mouths is rare.

A direct relationship exists between growth severity and plaque amount. Plaque removal and maintaining oral hygiene can reduce lesion severity. Growths cause aesthetic problems, chewing, speaking, driving problems, tissue traumas, secondary infections, and periodontal diseases. Treatment includes removing attachments on teeth, teaching proper brushing and flossing, and surgical procedures like gingivectomy and gingivoplasty. Patients should be informed about potential recurrence and the importance of plaque control. Gingival enlargements tend to resolve spontaneously within months after drug discontinuation. Changing the drug may be considered after medical consultation.

Oral Lesions Independent of Plaque

Common oral lesions in children include recurrent aphthous stomatitis, primary herpetic gingivostomatitis, recurrent herpes simplex infections, common oral candidiasis, angular cheilitis, and geographic tongue. The incidence rates are similar between children and adults.

Primary Herpetic Gingivostomatitis (PHG)

PHG is a viral disease caused by Herpes simplex virus (HSV) type-1, occurring acutely in early childhood, typically affecting children younger than 10 years, especially between 2 to 4 years old. In most cases (99%), there are no symptoms, or they are attributed to teething. The remaining 1% develop severe inflammation and ulceration of the lips and mucosa.

• Incubation Period: Approximately 1 week.
• Clinical Features: Fever, headache, cervical lymphadenopathy, diffuse inflammation, significant swelling, bleeding, and erythema in the marginal and attached gingiva.
• Ulceration: Vesicles burst, forming large ulcers.
• Symptoms: Difficulty chewing and swallowing due to severe pain. Adequate fluid intake is crucial to prevent dehydration.

PHG is infectious and typically regresses spontaneously within 12-20 days, healing without scarring within 10-14 days. Treatment focuses on preventing bacterial superinfections, requiring careful plaque removal. Acyclovir oral suspension (15 mg/kg) administered within the first 3 days has been reported to significantly reduce contagiousness and symptoms.

Candidiasis

Caused by an overgrowth of Candida albicans, an opportunistic fungus, which can reach rates of 50%-80% in the total mouth fungus population. It contains proteinase-containing strains that invade the keratinized epithelium. Generally transmitted from mother to infants during birth, its incidence increases with long-term antibiotic or steroid use in older children. It is also common in patients with diabetes, hypoparathyroidism, and those undergoing chemotherapy. HIV-infected children and adolescents are prone to oral candidiasis. Rarely seen on the gums in healthy individuals, it manifests in different types, such as pseudomembranous candidiasis (thrush), erythematous candidiasis, plaque type, and nodular forms. Clinically, it presents as diffuse, whitish patches easily removed from the mucosa. Topical treatments include antifungals like nystatin, amphotericin B, and miconazole.

Recurrent Herpes Simplex

Primary infections are usually transmitted by direct contact with a lesion or infected body fluids. HSV Type 1 infects the oral mucosa by binding to specific cell surface receptors. Post-primary infection, it settles in neuron ganglia via sensory and autonomic nerves, specifically the trigeminal ganglion, where it remains latent for life. Reactivation in the sensory ganglion causes recurrent herpetic infection, triggered spontaneously or by factors like sunlight, fatigue, emotional stress, trauma, fever, and immunosuppression. HSV type-1 is typically responsible for orofacial infections, found at a rate of 30-60% in children. Recurrent infections result from triggering factors, with herpes labialis being the most common. Lesions typically occur at the mucocutaneous junction, particularly on the lips, with symptoms like paresthesia, itching, pain, and burning sensation in 46-60% of patients. Lesions rapidly become vesicular, then burst into ulcers or crusted pustules.

Recurrent Aphthous Stomatitis (RAS)

The most common form of RAS in childhood is minor aphthae. Patients often refer to these ulcerative lesions as “cancers”. RAS lesions can range from 0.5 to 1.0 cm in diameter or appear as oval and irregular ulcers ranging in size from 1 to 3 mm. Small lesions heal in 7 to 10 days, while larger lesions take weeks to heal with scarring. Trauma, emotional stress, menstruation, nutrition, and endocrinopathies predispose the emergence of RAS. While there is no specific treatment, topical tetracycline, chlorhexidine gluconate or other mouthwashes, topical corticosteroids, or immunomodulators can be used in clinical management.

Angular Cheilitis

Inflammation beginning at the corners of the lips, leading to erosion, ulceration, and fissures, results in a very painful condition. Candida albicans and Staphylococcus aureus have been reported as causative agents. Angular cheilitis and other oral candidiasis infections are very common in HIV-infected children. Predisposing factors include immunodeficiency, vitamin B2 deficiency, decrease or loss of vertical dimension, and trauma.

Geographic Tongue (Benign Migratory Glossitis)

A benign inflammatory condition characterized by desquamation of superficial keratin and filiform papillae in the tongue, affecting approximately 1-2% of the population. Its etiology is unknown, although correlations with nutritional deficiencies and emotional stress have been suggested. Typically limited to the dorsum and lateral of the tongue, lesions may become symptomatic, causing a burning sensation. Symptoms can vary in severity. Patients may be advised to avoid acidic and spicy foods. Topical or systemic antihistamines can be used in treatment.

Periodontal Diseases in Childhood

Epidemiological studies show that all children and adolescents are affected by different forms of gingivitis. Bone and attachment loss is not common in children. However, the incidence of gingivitis in children 7 years and older is more than 70%. In epidemiological studies conducted in the USA, severe attachment loss in one or more teeth in children and young adults was found to be approximately 0.2-0.5%. Chronic periodontitis is more likely to occur in adults, while aggressive periodontitis is more common in children and adolescents.

Aggressive Periodontitis

Aggressive periodontitis is characterized by early onset, a familial tendency, and rapid attachment and bone loss. Main causes include pathogenic microflora, abnormalities in the host defense mechanism, phagocyte abnormalities, and a hypersensitive macrophage phenotype. It is divided into localized and generalized subgroups. The prevalence of the localized form, more common in young people, is between 0.1% and 15%. The rate of generalized aggressive periodontitis is 0.13% in the 14-17 age group.

Localized Aggressive Periodontitis (LAgP)

The disease typically begins around puberty, with attachment loss limited to two teeth in the interproximal areas, excluding the permanent first molars and incisors. Coexisting Aggregatibacter (Actinobacillus) spp., Bacteroides spp., and Eubacterium spp. are commonly found. Cases of LAgP are associated with defects in neutrophil function. The host response is severe, increasing destruction. Clinical examination shows low plaque and calculus amounts relative to inflammation severity. Patients do not show clinical signs of systemic diseases.

Generalized Aggressive Periodontitis (GAgP)

Primarily affects individuals under age 30, impacting the entire dentition and known as a disease of young adults. At least three permanent teeth other than the permanent incisors and permanent first molars must be affected. There is no strong antibody response as in LAgP. Affected teeth have a high proportion of Porphyromonas gingivalis in the subgingival flora. Neutrophil chemotaxis defects are observed.

Treatment of Aggressive Periodontitis

Successful results are obtained with systemic antibiotics, subgingival curettage, root surface straightening, and periodontal surgeries. Tetracycline alone or in combination with metronidazole gives very successful results. Amoxicillin-metronidazole may be preferred in younger children to avoid tetracycline-induced tooth discoloration. LAgP patients respond well to treatments, while GAgP patients may not respond as desired. Alternative antibiotics may be needed due to the pathogenic flora. Laboratory tests should be performed on plaque samples from GAgP patients to identify pathogens resistant to routinely used drugs. The presence of bone loss in primary teeth may be an early sign of localized aggressive periodontitis, warranting careful periodontal evaluation.

Chronic Periodontitis

Children are less susceptible than adults to this form of periodontitis, but it can rarely affect them and adolescents. The disease usually progresses at a low or moderate rate, with potential exacerbations. It is divided into localized (less than 30% of areas affected) or generalized (more than 30%). Classified by clinical attachment loss: mild (1-2 mm), moderate (3-4 mm), and severe (5 mm and above).

Progression requires a prior history of gingivitis, with key factors including increased pathological bacteria, immune system-related conditions, and genetic susceptibility. The approach involves eliminating inflammation, stopping progression, and stabilizing the oral environment. Treatment includes personal plaque control, periodontal initial treatments like detection, subgingival curettage, root surface straightening, and mouthwashes. Electric toothbrushes can be recommended for mentally or physically handicapped children and for children who cannot use brushes effectively.

Periodontitis as a Sign of Systemic Diseases

Systemic diseases causing periodontitis in children include hypophosphatasia, Papillon-Lefevre Syndrome, leukemias, Chediak-Higashi syndrome, histiocytosis X, Acrodynia, Down syndrome, AIDS, Leukocyte adhesion defect, neutropenia, and insulin-dependent diabetes. Defects in neutrophils and immune cell functions increase susceptibility to periodontitis and other infections. Can occur in localized or generalized forms with severe bone loss. Increased levels of periodontopathogens like A. actinomycetemcomitans, P. intermedia, E. corrodens, and Capnocytophaga are observed.

Necrotizing Periodontal Diseases

Characterized by acute pain in the interdental areas, necrosis, and crater-like ulceration. Lesions are covered by easily bleeding pseudo-membranes. Spirochete invasion and P. intermedia presence are noted on necrotic surfaces. Systemic findings like fever and lymphadenopathy may accompany it. Children are prone due to viral infections, nutritional deficiencies, systemic diseases, fatigue, and stress. Treatment includes antibiotics like metronidazole and penicillin for systemic findings. Mechanical debridement with ultrasonic devices is also used.

Conclusion

Periodontal diseases are common in children and adolescents. Bacterial plaque plays a primary role, but diseases affecting the host’s defense mechanism should be considered in early-onset cases. Dentists need sufficient knowledge of diagnostic features, occurrence, prevalence, microbiology, and treatment. Routine periodontal evaluations in childhood ensure early prevention. Early treatment, proper brushing instruction, and increased family awareness reduce disease prevalence.