Apical Periodontitis in Primary Teeth. Etiology, Pathogenesis, Diagnostics.

Periodontium in Children

The periodontal ligament (PDL) in primary teeth and permanent teeth with immature roots is characterized by a looser connective tissue structure, containing a higher density of cellular elements and blood vessels. Unlike the stable and well-defined architecture of adult PDL, the PDL in children remains in a state of dynamic development and adaptation.

By age three, the PDL of primary teeth begins to exhibit Sicher’s plexus—a network of fiber bundles oriented parallel to the tooth’s long axis. This plexus facilitates the vertical movement of teeth during eruption. As the dentition transitions to mixed dentition (around age 9), these fibers shift to a 45° inclination relative to the tooth’s axis. By the permanent dentition phase (age 14), the dominance of these fibers diminishes, marking the maturity of PDL structures.

In teeth with incomplete root formation, the periodontal space is observable only in the formed root segments. In erupting teeth, this space appears widened near the cervical region. Notably, in children and adolescents, the periodontal gap is nearly twice as wide as that in adults, reflecting the immature and adaptive state of their periodontium.

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Cementum Development and Its Age-Dependent Variations

• Primary Teeth: Acellular cementum predominantly covers the root surface, with cellular cementum appearing only in the apical third.
• Mixed Dentition: The resorption of primary root structures triggers an increase in cellular cementum, which can extend to cover half the root length by ages 10–11.
• Permanent Teeth: Mature permanent roots are covered mostly by acellular cementum (approximately two-thirds of the root), with cellular cementum limited to the apical third.

Collagen fiber bundles of the PDL integrate deeply into the cementum, contributing to the root's structural integrity.

The alveolar bone in children contains a higher ratio of organic to mineral components compared to adults, rendering it less resistant to external stimuli. Its trabecular pattern is coarser, with wide Haversian canals and red marrow dominating the structure. During the mixed dentition stage, the bone's radiographic appearance remains poorly differentiated and coarse.

As permanent teeth erupt, the interdental septa undergo resorption and remodeling, eventually acquiring distinct compact plates. Final mineralization of these structures occurs alongside the closure of the root apex, typically by ages 8–9 in the anterior regions and 14–15 in the posterior.

Unique Anatomical Features of Primary Teeth

1. Thinner enamel and dentin layers in primary teeth (~1 mm), with uniform enamel thickness across the crown.
2. Broader mesiodistal dimensions relative to crown height.
3. Convergent crown surfaces towards the occlusal plane, narrowing the vestibulo-oral dimension in primary molars.
4. Larger pulp chambers and thinner root structures in primary teeth.
5. Presence of additional root canals in primary molars, often extending from the pulp chamber to the cementum surface.

Etiology

Apical Periodontitis is an inflammatory process affecting the periapical tissues of a tooth. It can result from infectious, toxic, allergic, or traumatic causes. This condition is characterized by the necrosis of the dental pulp and the destruction of surrounding bone tissue.

Apical periodontitis arises primarily due to bacterial invasion of the root canal system. Clinical evidence supports that periapical inflammation and bone resorption occur only when microorganisms infiltrate necrotic pulpal tissue.

When the tooth pulp is exposed, microorganisms from saliva and dental plaque, predominantly anaerobic bacteria, colonize the root canal. These organisms contaminate not only the main root canal but also lateral canals, apical deltas, and dentinal tubules. Key microbial species associated with apical periodontitis include:

• Bacteroides forsythus
• Campylobacter showae
• Fusobacterium nucleatum
• Actinobacillus actinomycetemcomitans
• Porphyromonas gingivalis
• Prevotella intermedia
• Treponema denticola

Periapical inflammation may also result from procedural errors during endodontic treatment, including overextension of instruments or excessive application of medicaments. Instrumentation beyond the apical foramen can damage periapical tissues, potentially triggering acute inflammation. In the absence of infection, such trauma may resolve with complete tissue regeneration. However, if microbial contamination is present, this breach facilitates the spread of infection.

Antiseptics, such as those containing phenolic or aldehyde compounds, can irritate periapical tissues, leading to necrosis and exudate formation. Similarly, some root canal sealers exhibit an initial cytotoxic effect, which subsides as the material sets, allowing for eventual tissue recovery if infection is absent.

The Main Causes of Apical Periodontitis in Primary Teeth:

1. Acute or Chronic Pulpitis

The tooth may present with a carious cavity or be previously filled. In cases of chronic pulpitis, infection spreads from the pulp through the apical foramen and accessory canals to the periodontium, particularly in the furcation area. This occurs due to the anatomical and histological characteristics of the roots of primary teeth and the close connection between the pulp and periodontium.

       2. Overdose or Prolonged Exposure to Devitalizing Agents

When devitalizing agents are used in treating pulpitis, an overdose or prolonged exposure can harm the periodontium, potentially leading to apical periodontitis.

       3. Trauma to the Periodontium

During pulp extirpation or root canal treatment, trauma to the surrounding periodontal tissues can result in inflammation and subsequent apical periodontitis.

       4. Extrusion of Filling Material Beyond the Root Apex

If filling material is inadvertently pushed beyond the apex during pulpitis treatment, it can irritate the periodontium and cause inflammation.

       5. Use of Potent Antiseptics

The application of strong antiseptics during treatment may negatively affect the delicate balance of the periodontium, leading to apical periodontitis.

       6. Pushing Infectious Contents Beyond the Root Apex

Pushing infected material from the root canal beyond the apex exacerbates inflammation, potentially leading to apical periodontitis.

       7. Allergic Reactions to Bacterial Byproducts and Medications

The periodontium may react adversely to bacterial byproducts or certain medications, leading to inflammation and infection at the apex of the tooth.

       8. Mechanical Overload of the Tooth

Conditions like orthodontic treatment, an excessive bite on a filling, or harmful habits such as biting hard objects can stress the tooth and its periodontium, contributing to apical periodontitis.

       9. Acute Dental Trauma

A sudden injury to the tooth can directly affect the pulp and periodontium, leading to inflammation and the development of apical periodontitis.

ICD-10-CM Classification

K04.4 Acute apical periodontitis of pulpal origin

K04.5 Chronic apical periodontitis

K04.6 Periapical abscess with sinus

K04.7 Periapical abscess without sinus

K04.8 Radicular cyst

K04.9 Other and unspecified diseases of pulp and periapical tissues

K04.90 Unspecified diseases of pulp and periapical tissues

K04.99 Other diseases of pulp and periapical tissues

Pathogenesis

Apical periodontitis is most commonly chronic, representing a balance between microbial activity and the host's immune defenses. Bacteria within the root canal and dentinal tubules remain protected from immune surveillance, proliferating and releasing metabolic by-products that damage periapical tissues. Even microorganisms with low virulence can perpetuate chronic inflammation in these protected environments.

Key mechanisms include:

1. Bacterial Cytotoxicity

Certain bacteria, such as Actinobacillus actinomycetemcomitans, produce toxins (e.g., leukotoxins, collagenases, and lipopolysaccharides) that:

• Destroy neutrophils and monocytes.
• Inhibit fibroblast activity and promote bone resorption.
• Induce immune dysfunction, allowing persistent inflammation.

       2. Immune Response

• Specific Immunity: Bacterial antigens stimulate T- and B-lymphocytes, activating immune cascades.
• Non-Specific Immunity: Lipopolysaccharides activate macrophages to release mediators like cytokines, which amplify tissue destruction.

Antigen-antibody complexes within the root canal can also exacerbate bone resorption by recruiting neutrophils and promoting inflammatory mediator release.

In acute apical periodontitis, neutrophils and exudate dominate the response. Proteolytic enzymes from these cells contribute to tissue breakdown, abscess formation, and elevated pressure in the periapical region. This inflammatory pressure can lead to submucosal or subcutaneous abscess formation if the exudate breaches periosteal barriers.

Chronic periodontitis in children is typically a primary, chronic condition, which often progresses asymptomatically and is only detected during dental checkups.

Children rarely complain of discomfort, but parents may notice the presence of a fistula on the gum. Upon examination, the tooth may appear carious or previously filled, with the crown showing signs of discoloration, it is becoming duller, with a grayish or brownish tint, particularly near the tooth’s neck. The tooth does not respond to thermal stimuli. Probing may reveal a communication with the tooth’s pulp chamber, yet probing the floor or walls of the cavity and its communication is generally painless. Percussion is also painless. In cases of significant bone destruction, percussion may produce a dull sound, and the tooth may show mobility.

Granulations may sometimes be found in the canals or pulp chamber of teeth that were started but not completed due to factors beyond the dentist's control, or where fillings have fallen out. In such cases, bleeding may be observed from the tooth's cavity, and children may experience pain while chewing.

In periapical abscess with or without sinus, the clinical symptoms most prominently affect the gum and alveolar ridge. On examination, there is often swelling, hyperemia, and a puffy appearance of the gum mucosa, with a fistulous tract discharging pus or protruding granulations. If the tooth has formed and the pathological process is localized near the apex, the fistula will be closer to the mucogingival fold. If the roots are resorbed, or the process is centered in the furcation area, the fistula will be located closer to the marginal edge.

The primary diagnostic method for chronic periodontal inflammation is radiographic imaging. It helps to identify the lesion’s location, determine the type and extent of the inflammation, assess the condition of surrounding bone structures, and stage the root's development.

Diagnostics

Accurate diagnosis begins with a thorough review of the patient’s medical and dental history. Systemic conditions significantly influence treatment planning. For instance, children with systemic diseases, such as congenital heart conditions with a risk of infective endocarditis or those with immunodeficiencies, require careful management. In such cases, all primary teeth with apical periodontitis should be extracted to prevent potential complications.

The diagnosis of apical periodontitis in a primary tooth is made based on clinical findings:

• Clinical Signs: The presence of caries or discolored teeth, a fistula, or scar tissue (either from patient complaints or during preventive examination).
• Patient History: The tooth has likely been treated previously for caries or pulpitis. The patient may report past pain while biting or swelling of the cheek or gum near the affected tooth.
• Clinical Examination: Changes in the tooth crown’s color and the presence of a fistula on the gum. There may also be signs of hyperemia or cyanosis of the mucosa around the root projection area. The tooth may show mobility in cases of significant bone destruction or root resorption. No pain is typically felt when probing the bottom, walls, or communicating areas of the tooth.

The evaluation of pulp status in children presents unique challenges due to their behavior and developmental stages:

Electroodontometry: This diagnostic tool is often unreliable in primary teeth and immature permanent teeth. Anxiety, fear, and communication barriers can distort results.

Thermal Tests: These are also generally unsuitable for primary teeth, as they fail to yield consistent or accurate outcomes.

Percussion Sensitivity: Although percussive sensitivity is a hallmark of apical periodontitis, it is less effective in diagnosing the condition in primary teeth of young children.

Radiological Findings: Intraoral radiographs of high quality are essential for diagnosis. They offer crucial insights into the periapical region and help achieve several diagnostic objectives:

Assessment of Root Development: Identifying the stage of root formation, the extent of resorption, and the presence of external or internal root resorption.

Evaluation of Permanent Tooth Follicles: Determining the integrity of the cortical plate surrounding the follicle of the permanent tooth.

Pathological Mapping: Locating and measuring the size and position of pathological lesions in periapical tissues.

Determining Working Length: Essential for planning endodontic procedures if indicated.

In pediatric dentistry, mainly periapical X-rays are used to assess primary teeth, while CBCT scans are more commonly employed for detailed evaluation of the pulp and root canal systems in permanent teeth.

In chronic periodontitis, radiographs show widening of the periodontal space, usually limited to a specific area or, rarely, the entire length of the root, depending on the extent of the process. Cementum may appear thickened, manifesting as a deformity of the root, such as a club-shaped or tapered enlargement at a particular root segment. Periapical abscess is characterized by areas of bone radiolucency with unclear borders.

Radiographic findings, in conjunction with clinical assessments, provide a reliable foundation for diagnosing apical periodontitis and tailoring treatment to the child’s unique needs and health status.

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Complications

Depending on the type and intensity of inflammation in the periodontal tissues of the primary tooth, as well as the stage of development of the permanent tooth follicle, the following complications may arise:

• Follicular Death: Occurs if the inflammatory process begins before the mineralization of the permanent tooth.
• Local Hypoplasia (Turner’s Tooth): If exudate penetrates the permanent tooth follicle during the early stages of enamel mineralization, it can lead to localized enamel defects.
• Tooth Germ Sequestration: The death of tissues forming the tooth may result in the sequestration of the tooth germ.
• Premature Eruption: The premature eruption of the permanent tooth may occur as a consequence of the inflammatory process.
• Spread of Pathology: The pathological process may extend to adjacent teeth and permanent tooth follicles.
• Cyst Formation: Radicular or follicular cysts can form due to the inflammatory process.
• Displacement of Tooth Germs: The development of permanent teeth may be disrupted, leading to displacement, retention, and eruption anomalies.

Treatment Methods

Addressing apical periodontitis in primary teeth is one of the challenges in pediatric restorative dentistry due to the unique morphology of primary teeth and the difficulties in diagnosing this condition. The main treatment approaches are:

• surgical (tooth extraction)
• conservative (pulpotomy or pulpectomy)

Absolute Indications for Surgical Treatment of Primary Teeth

Tooth extraction is indicated in the following cases:

• Root resorption exceeding one-third of its length.
• Loss of functional value of the tooth.
• Perforation of the tooth floor.
• Spread of the pathological process to the developing permanent tooth germ.
• Radiographic evidence of internal root resorption.
• Presence of odontogenic or follicular cysts.
• Severe systemic conditions (e.g., congenital heart defects, leukemia, tumors, immunodeficiencies, or during immunosuppressive therapy).
• Less than 1.5 years remaining until the tooth naturally exfoliates.
• Inadequate patient cooperation, where treatment under general anesthesia is not feasible.

Goals of Conservative Treatment

The primary objective of conservative management for apical periodontitis in primary teeth is:

• Elimination of inflammation in the periapical tissues.
• Restoration of the tooth's functional value.

Pulpectomy Technique in Primary Teeth

In cases where the pulp has undergone necrosis, the pulpectomy procedure involves the complete removal of the necrotic pulp followed by filling the root canals with resorbable material. This ensures compatibility with the natural resorption process of primary teeth.

All endodontic treatments are performed using a rubber dam to ensure isolation and maintain aseptic conditions.

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