Periodontitis

Etiology (Causes) of Apical Periodontitis

Based on its origin, apical periodontitis is primarily divided into three categories:

1. Infectious periodontitis
2. Traumatic periodontitis
3. Drug-induced (medicamentous or chemical) periodontitis

Infectious Apical Periodontitis

This is the most common form and typically occurs when microorganisms (such as Staphylococcus aureus and albus, non-hemolytic and hemolytic streptococci, fusobacteria, spirochetes, and occasionally fungi), their toxins, and products of pulp and dentin decay penetrate the periodontium from an infected root canal or, less commonly for apical periodontitis, from a deep periodontal pocket (which primarily relates to marginal periodontitis).

According to the pathway of bacterial penetration, infectious periodontitis can be classified as:

• Intradental: Microorganisms enter the periapical tissues from within the tooth, usually from an infected or necrotic pulp secondary to dental caries, or via the root canal during or after endodontic (root canal) treatment. This is the predominant pathway for apical periodontitis.
• Extradental: Less common for primary apical periodontitis, this involves infection spreading from surrounding tissues. Examples include:
  • Contiguous spread from osteomyelitis, osteitis, periostitis of the jaw.
  • Spread from adjacent sinusitis (inflammation of paranasal sinuses) or rhinitis.
  • Spread from severe marginal periodontitis affecting the apex.
  • Hematogenous (via bloodstream) or lymphogenous (via lymphatics) spread from distant infections like tuberculosis, hepatitis, typhoid fever, or influenza is theoretically possible but very rare as a primary cause of apical periodontitis.

Traumatic Apical Periodontitis

Traumatic apical periodontitis occurs when the periapical tissues are injured. This can be due to:

• Acute Trauma: A direct blow to the tooth, a bruise, a fall, a forceful push, or accidentally biting on hard objects. Acute trauma often causes relatively quickly resolving irritation of the periodontium. However, sometimes these injuries are accompanied by hemorrhage within the pulp or disruption of its blood supply at the apex, followed by pulp necrosis. This condition might not manifest symptoms for a long time, only presenting with a change in tooth color (discoloration) and a lack of sensitivity to various stimuli (thermal, electrical).
• Chronic Microtrauma (Occlusal Trauma): A high filling, an artificial crown that overestimates the bite (occlusal prematurity), or parafunctional habits like bruxism can cause repeated minor trauma to the periodontium, leading to the development of chronic traumatic periodontitis.
• Iatrogenic Trauma (during dental procedures): Injury to the periapical tissues by endodontic instruments (files, reamers) extending beyond the apical foramen, or by pushing root canal filling materials, a pin, or irrigants through the apical opening during root canal treatment.

Drug-Induced (Medicamentous/Chemical) Apical Periodontitis

This form can occur as a result of potent chemical or medicinal substances unintentionally entering the periapical periodontium during dental treatment. Examples include:

• Strong root canal irrigants or disinfectants (e.g., arsenous acid - historically used for pulp devitalization, phenol, formalin-containing compounds).
• Extrusion of root canal filling materials beyond the apex, such as phosphate cement, resorcinol-formalin pastes, zinc-eugenol pastes, or parts of a post/pin.
• Local immunological reaction (hypersensitivity) in response to certain dental materials or medications placed within the root canal or contacting periapical tissues, such as some antibiotics, eugenol, chloramine, chlorhexidine, dimexide, or iodine preparations if extruded beyond the apex.

Pathogenesis (Development) of Apical Periodontitis

The development of periodontal inflammation at the root apex is intricately linked to the entry of infectious and/or toxic contents from the root canal system into the periodontal ligament space. An irritating agent—be it bacteria (cocci, bacilli, etc.), their metabolic products (toxins, enzymes), or certain medications—is required to initiate the process. Endotoxins, particularly lipopolysaccharide (LPS) from the cell walls of Gram-negative bacteria colonizing necrotic root canals, play a significant role. These endotoxins have potent toxic and pyrogenic (fever-inducing) effects.

Once these irritants reach the periapical tissues, a cascade of inflammatory and immune responses is triggered:

1. Cellular Damage and Enzyme Release: There is often multiple damage to connective tissue cells (fibroblasts, osteoblasts, cementoblasts) and a massive release of lysosomal enzymes from these damaged cells and from inflammatory cells (neutrophils, macrophages).
2. Mast Cell Degranulation: Endotoxins trapped in the periapical tissues lead to the degranulation of mast cells, which are a source of potent inflammatory mediators like heparin and histamine.
3. Increased Vascular Permeability: Biologically active components (histamine, bradykinin, prostaglandins, leukotrienes) cause a sharp increase in the permeability of local blood vessels. This results in edema (fluid accumulation) and an increase in cellular infiltration (influx of inflammatory cells).
4. Microcirculatory Disturbances: Blood flow is disrupted, leading to stasis, thrombosis (clot formation in small vessels), hyperfibrinolysis (excessive breakdown of fibrin), and secondary hypoxia (oxygen deprivation) in the tissues. This hypoxia leads to depolymerization of the ground substance of the connective tissue.
5. Impaired Tissue Trophism: As hypoxia increases, tissue nutrition (trophism) is severely disturbed. Cells are unable to receive adequate oxygen and nutrients from the compromised ground substance and, conversely, cannot effectively eliminate waste products. This leads to "slagging" (accumulation of metabolic waste) in both cells and the intercellular substance, further exacerbated by vascular wall dysfunction.
6. Immune System Activation: Bacterial endotoxins also activate components of the complement system, leading to the formation of more biologically active substances that enhance vascular permeability and chemotaxis (attraction of inflammatory cells). This results in the accumulation of mononuclear lymphocytes and macrophages.
7. Bone Resorption: Activated macrophages and other immune cells secrete enzymes (e.g., collagenase, prostaglandins) and cytokines (e.g., IL-1, TNF-α) that stimulate osteoclast activity. Osteoclasts are cells responsible for bone resorption, leading to the destruction of alveolar bone tissue around the root apex, which is visible radiographically as a periapical radiolucency.

The classic signs of inflammation—local temperature rise, pain, edema, hyperemia (redness), and dysfunction (e.g., pain on biting)—become manifest. The tissue becomes more permeable due to the formation of voids in the ground substance, and its protective function is compromised.

Classification of Apical Periodontitis

In the practice of therapeutic dentistry, various classifications of apical periodontitis are used to characterize the nature and stage of the disease, which helps in treatment planning. A common clinical classification is as follows:

1. Acute Apical Periodontitis:
   • Initial Phase (Phase of Periapical Intoxication): Early stage with mild inflammation, primarily due to toxins.
   • Exudative Phase: Characterized by the accumulation of inflammatory exudate.
     • Serous Exudation: Predominantly serous (watery) fluid.
     • Purulent Exudation: Formation of pus (suppuration). This can progress to an acute apical abscess.
2. Chronic Apical Periodontitis: Long-standing inflammation, often asymptomatic or with mild, intermittent symptoms.
   • Chronic Apical Fibrous Periodontitis: Characterized by the formation of fibrous scar tissue in the periapical region, often seen as a slight widening of the periodontal ligament space on radiographs. Usually asymptomatic.
   • Chronic Apical Granulating Periodontitis: Characterized by the formation of granulation tissue (a highly vascular inflammatory tissue) at the apex. This can lead to bone resorption and may be associated with a draining sinus tract (fistula). Often asymptomatic or mildly symptomatic.
   • Chronic Apical Granulomatous Periodontitis (Periapical Granuloma): Characterized by a well-circumscribed mass of chronically inflamed granulation tissue encapsulated by fibrous tissue at the root apex. May be asymptomatic or become symptomatic if it transforms into a cyst or becomes acutely infected. Radiographically appears as a well-defined radiolucency.
     • A periapical granuloma can sometimes undergo cystic degeneration, forming a radicular cyst (periapical cyst).
3. Chronic Apical Periodontitis in an Acute Stage (Exacerbation of Chronic Apical Periodontitis / Phoenix Abscess): This occurs when a pre-existing chronic apical lesion becomes acutely inflamed and symptomatic.
   • Chronic apical fibrous periodontitis in the acute stage.
   • Chronic apical granulating periodontitis in the acute stage.
   • Chronic apical granulomatous periodontitis in the acute stage (e.g., an infected granuloma or cyst).

Clinical Symptoms and Diagnosis of Apical Periodontitis

Acute Apical Periodontitis: Phases and Symptoms

The main symptom of acute apical periodontitis is persistent, localized pain. The nature and severity of this pain, along with other local and general manifestations, depend on the stage of inflammation and whether serous or purulent exudate has accumulated at the root apex.

Clinical manifestations of acute apical periodontitis are primarily due to the phase of acute periodontal inflammation. Two main phases are recognized:

1. Intoxication Phase (Initial Phase / Periapical Irritation):
   • Patient Complaints: Constant, localized pain of varying intensity (often mild to moderate, dull, or aching), which is aggravated by biting on the tooth (occlusal pressure) or touching it. The patient can always accurately identify the affected tooth.
   • Objective Findings: The face appears symmetrical, and mouth opening is usually free. The mucous membrane in the projection of the affected tooth's apex is typically pale pink and normal in appearance. The tooth crown may not be discolored; there might be a carious cavity or a permanent filling present. Percussion (tapping) of the tooth is slightly painful, indicating increased sensitivity of the periapical periodontium. No swelling is usually present.
2. Exudation Phase: At this stage, the severity of inflammatory symptoms depends on the nature of the exudate (serous or purulent).
   • Patient Complaints: Continuous pain, which can remain at the same level or intensify. The patient accurately points to the affected tooth. A characteristic sensation is that the tooth feels "extruded," "raised," or "grown" out of its socket. Pain is elicited upon biting or even light touching of the tooth.
   • Objective Findings:
     • Percussion is painful, initially more so in the vertical direction (along the long axis of the tooth), and then also in the horizontal direction.
     • The tooth may exhibit slight mobility. It is not usually changed in color at this stage unless the pulp has been necrotic for some time.
     • Often, the crown of the tooth is intact, or if a carious cavity is present, probing of the walls and bottom of the carious cavity is typically painless (as the pulp is usually necrotic).
     • The cavity of the tooth (pulp chamber) is usually not open to the oral cavity. If it is opened (e.g., during access preparation), necrotic, decomposed pulp tissue is observed in the pulp chamber and root canals.
     • The mucous membrane in the projection of the diseased tooth's apex (apical mucosa) is hyperemic (red) and edematous (swollen). Palpation of this area is painful.

The exudation phase is characterized by all five classic signs of inflammation: local fever (increased temperature of surrounding tissues), pain, edema, hyperemia, and dysfunction (e.g., inability to chew on the tooth). The progression of an acute inflammatory process at the stage of exudation can lead to significant collateral edema of the surrounding peri-maxillary soft tissues (e.g., facial swelling). Regional lymph nodes (submandibular, submental) may be unchanged or slightly enlarged on the side of the diseased tooth; if enlarged, they are typically mobile and may or may not be tender on palpation. Body temperature is usually normal or slightly elevated. The general condition of the patient is often not significantly disturbed in the serous phase.

The serous phase of acute periodontitis can transition into a purulent phase (suppurative acute apical periodontitis), which may last about 2-20 days if untreated or if drainage is not established. The clinical picture becomes more pronounced and severe:

• Pain intensifies, becomes throbbing or pulsating, and is most often continuous. It may radiate along the branches of the trigeminal nerve.
• Pain is especially aggravated by touching the tooth, leading the patient to keep their mouth slightly open to avoid contact with opposing teeth.
• The condition of the affected tooth is similar to that in serous acute apical periodontitis regarding discoloration and crown integrity (may be intact or carious). The pulp chamber, if accessible, contains necrotic pulp.
• The affected tooth is often pathologically mobile, and percussion is sharply painful.
• The mucous membrane of the transitional fold (vestibular fornix), palate, or sometimes the alveolar process on the lingual/palatal surface in the area of the affected and adjacent teeth is markedly edematous and hyperemic. This swelling may be fluctuant if pus has accumulated subperiosteally.
• Regional lymph nodes (submandibular, chin, less often buccal) are typically enlarged, painful on palpation, and mobile.
• Systemic symptoms like fever, malaise, and leukocytosis are more common and pronounced.

These phenomena tend to increase with the accumulation of purulent exudate within the confined periodontal ligament space. The excruciating pain can last for several days. As soon as the purulent exudate finds a pathway out (e.g., through the root canal if open, through a draining sinus tract/fistula onto the mucosa or skin, or by spreading through the periosteum), the pain syndrome often weakens. If the infection spreads beyond the immediate periapical area, complications of acute purulent apical periodontitis can develop, such as acute odontogenic periostitis ("dental abscess" in common terms), or in more advanced cases, cellulitis or phlegmon of the peri-maxillary fascial spaces, or acute odontogenic osteomyelitis (infection of the jaw bone).

Chronic Apical Periodontitis (Brief Overview)

Chronic forms of apical periodontitis (fibrous, granulating, granulomatous) are often asymptomatic or cause only mild, intermittent symptoms such as slight tenderness to percussion or pressure. They are frequently discovered incidentally on dental radiographs taken for other reasons. An acute exacerbation of a chronic lesion (Phoenix abscess) will present with symptoms similar to acute apical periodontitis.

Treatment of Apical Periodontitis

General Objectives of Treatment

The primary objects of intervention in the treatment of apical periodontitis are the infected or contaminated root canal system (including its main canal(s) and numerous branches/ramifications and dentinal tubules which can harbor microflora) and the inflamed periodontal tissues at the root apex. The main goals are to:

1. Eliminate infection from the root canal system.
2. Remove irritants (necrotic pulp tissue, bacteria, toxins).
3. Create an environment conducive to the healing of periapical tissues.
4. Prevent reinfection by providing a hermetic seal of the root canal system.
5. Restore the tooth to form and function.

Treatment of Acute Apical Periodontitis

Treatment depends on the phase of inflammation:

1. Treatment in the Intoxication Stage (Initial Phase): This is typically performed in one visit.
   • Anesthesia: Effective local anesthesia is administered (e.g., using modern highly effective anesthetics like 4% articaine with epinephrine – Ultracaine, Alfacaine, Septanest, or 2% lidocaine solution). To enhance the analgesic effect and prolong the action, a vasoconstrictor like 0.1% epinephrine hydrochloride solution (e.g., 1 drop per 10-15 ml of anesthetic, or pre-mixed formulations) can be added. However, vasoconstrictors must be used with caution or are contraindicated in patients with certain cardiovascular diseases, uncontrolled diabetes mellitus, hyperthyroidism, or in some elderly patients.
   • Access and Cavity Preparation: Removal of any existing dressing or old filling, and preparation of the carious cavity to gain access to the pulp chamber.
   • Opening of the Tooth Cavity (Access Cavity): Creating wide and convenient straight-line access for instruments to the pulp chamber and the orifices (mouths) of the root canals.
   • Expansion of Root Canal Orifices.
   • Chemo-Mechanical Debridement: Evacuation of necrotic pulp tissue (disintegration products) from the root canal(s). This work with all endodontic instruments (files, reamers) should be carried out incrementally, using techniques like parietal filing (against the canal walls) and balanced force or half-turned motions to effectively clean and shape the canals. Copious irrigation is essential.
   • Drug Treatment (Irrigation) of the Root Canal: Using appropriate antimicrobial irrigants. These should be non-irritating to periapical tissues if extruded. Examples include:
     • Sodium hypochlorite (NaOCl) solution (e.g., 0.5% to 6%), heated to around 40°C (enhances efficacy).
     • Chlorhexidine gluconate solution (e.g., 0.06% to 2%).
     • Sterile saline or local anesthetic solution for final rinse.
     • Historically, solutions like 0.1% potassium permanganate, 0.02% furacilin, or 0.1% dimexide were used, but NaOCl and chlorhexidine are current standards.
     After drug treatment (irrigation and shaping), the root canal is thoroughly dried using dry sterile paper points of an appropriate size, or historically, cotton tampons on a root needle.
   • Root Canal Filling (Obturation): The cleaned, shaped, and dried root canal system is filled with a biocompatible material to provide a three-dimensional seal, preventing reinfection. Common materials include gutta-percha with a sealer cement. Completion of this procedure should be verified with a postoperative X-ray (radiographic control) to assess the quality and extent of the fill.
   • Permanent Coronal Seal: Placement of a permanent filling or restoration in the access cavity to seal the tooth coronally and restore its form and function.
2. Treatment in the Phase of Exudation (Serous or Purulent): This is often carried out in two or more visits.
   • First Visit (Emergency Drainage and Debridement):
     • Anesthesia is administered.
     • Preparation of the carious cavity (if present) or trepanation (drilling an access opening) of the intact crown of the tooth is performed with a turbine handpiece.
     • The pulp cavity is opened, and the orifices of the root canals are located and widened.
     • Necrotic pulp tissue is removed from the root canal(s).
     • Crucially, an attempt is made to establish drainage through the root canal by passing small files through the apical foramen (apical opening) to relieve pressure from accumulated exudate. The criterion for controlling the opening of the apical foramen is the appearance of exudate (serous fluid or pus) in the lumen of the root canal.
     • In many cases during the first emergency visit, the tooth is left open for drainage for a short period (e.g., 24-48 hours). The patient is warned to insert a small cotton swab into the tooth before eating to prevent food impaction, and after eating, to remove the cotton swab and rinse the mouth with water. (Note: Leaving teeth open for extended periods is controversial and generally discouraged in modern endodontics due to risk of bacterial contamination from the oral cavity, but may be done for short-term emergency drainage.)
     • If apical periodontitis is complicated by acute odontogenic periostitis (swelling, hyperemia and edema of the mucous membrane, painful palpation and smoothness of the transitional fold in the area of the diseased tooth), an increase in body temperature, or changes in the blood formula, then a course of systemic broad-spectrum antibiotics and desensitizing drugs (antihistamines) is prescribed. Concurrently, if there's a fluctuant subperiosteal abscess, an incision and drainage (I&D) procedure is performed along the transitional fold, dissecting the periosteum, and the wound is drained (e.g., with a rubber or gauze drain).
   • Second Visit (and subsequent, if needed):
     • Anamnesis is collected (inquiring if the tooth still hurts, if there was pain when chewing).
     • Objective status is assessed: state of the surrounding mucous membrane, regional lymph nodes, percussion data, presence or absence of exudate in the root canal, any sinus tract healing.
     • If the patient has no complaints and the general and local condition is satisfactory (no swelling, pain, or exudate), then chemo-mechanical debridement of the root canal system proceeds. This involves thorough cleaning, shaping, and irrigation with solutions of proteolytic enzymes (to dissolve organic debris - less common now) and antiseptics.
     • If infection and symptoms persist, intracanal medicaments (e.g., calcium hydroxide paste) may be placed for a period (e.g., 1-4 weeks) to further disinfect the canal system before final obturation.
     • Once the canal is deemed clean and asymptomatic, it is degreased, dried, and obturated (sealed). A control X-ray is taken to confirm the quality of the root canal filling. A permanent coronal restoration is then placed.

Treatment of Chronic Forms of Apical Periodontitis

The goal of treating chronic apical periodontitis is to eliminate the root canal as a source of periapical inflammation and to actively influence (promote healing of) the destructive processes in the periapical tissues. Treatment of any form of chronic apical periodontitis, if non-surgical root canal therapy is chosen, is often indicated to be completed in one or two visits, provided the canal can be adequately disinfected and dried:

1. Access and Cavity Preparation: Preparation of a carious cavity (if present) in compliance with all rules and stages, or creation of an access cavity through an intact crown.
2. Opening of the Tooth Cavity (Pulp Chamber).
3. Widening the Orifice(s) of the Root Canal(s) and creating good, straight-line access into them.
4. Chemo-Mechanical Debridement: Removal of putrid masses, necrotic pulp remnants, and infected dentin from the root canal system under an antiseptic "bath" (copious irrigation) using the entire range of endodontic instruments (files, reamers, ultrasonic tips). Working length is determined with an apex locator and/or radiographs.
5. Degreasing and Dehydrating the Walls of the Root Canal: After thorough cleaning and shaping, the canal walls are dried. For this purpose, modern dentistry recommends the use of specific drying agents or protocols (e.g., irrigation with alcohol or specific solutions like Netispad, Styptic, Largal ultra, Canal plus - some of these may be historical or regional product names; current practice emphasizes thorough drying with paper points after final irrigation with NaOCl and often EDTA).
6. Root Canal Filling (Obturation): Filling the root canal system up to the physiological apex (typically 0.5-1mm short of the radiographic apex). This is followed by a postoperative X-ray to confirm the quality (density, length, apical seal) of the root canal obturation. Filling of the root canal with hardening pastes (sealers) and a core material like gutta-percha is the standard of care. The first portion of the filling material (sealer) is introduced into the root canal, often at the tip of a file or Lentulo spiral, and brought under gentle pressure towards the apex of the tooth root, sometimes using a pre-fitted gutta-percha point or by coating the master cone, which aims for effective obturation of the apical third. Subsequent portions of gutta-percha and sealer are then condensed into the canal using various techniques (e.g., lateral condensation, warm vertical compaction).
7. Permanent Coronal Filling/Restoration: After successful root canal obturation, a permanent restoration (filling, onlay, crown) is placed to seal the tooth coronally and restore its function and aesthetics. This is critical to prevent reinfection of the root canal system.

In some cases of chronic apical periodontitis, particularly large lesions or those unresponsive to non-surgical treatment, surgical endodontic treatment (apicoectomy or periapical surgery) may be indicated. This involves surgically accessing the root apex, removing the apical portion of the root and the associated pathological tissue, and placing a retrograde filling in the root end.

Dispensary Observation (Follow-Up)

Patients treated for destructive forms of apical periodontitis (granulating, granulomatous, cystic) are typically registered for dispensary observation (follow-up). Repeated clinical and radiographic examinations are carried out at intervals, for example, after 3, 6, and 12 months, and then annually or as indicated.

If, upon examination after 12 months (or longer, depending on lesion size and healing rate), the patient presents no complaints, and no pathological changes (or signs of healing/resolution of the previous lesion) are found on the radiograph in the periapical region, then further routine intensive observation may not be required, and the patient can be removed from active dispensary follow-up for that specific tooth, transitioning to regular dental check-ups.

If, after 12 months or more, even in the absence of patient complaints, radiological examination still determines persistent or enlarging destruction of the periapical tissues, or if symptoms recur, then repeated endodontic treatment (non-surgical retreatment, involving removal of the old root filling, further chemo-mechanical debridement, and re-obturation) or surgical endodontic treatment is required.

Differential Diagnosis of Apical Periodontitis

Apical periodontitis needs to be differentiated from other conditions causing dental pain or periapical changes:

Complications and Prevention

Untreated apical periodontitis can lead to:

• Acute apical abscess formation.
• Spread of infection to adjacent tissues (cellulitis, osteomyelitis of the jaw).
• Formation of a dental sinus tract (fistula) draining onto the mucosa or skin.
• Development of a radicular (periapical) cyst.
• Tooth loss.
• Rarely, systemic spread of infection (e.g., bacteremia, cavernous sinus thrombosis, Ludwig's angina if mandibular molar involved).

Prevention primarily involves:

• Preventing dental caries through good oral hygiene, diet, and fluoride.
• Early detection and treatment of dental caries before pulp involvement.
• Prompt and effective endodontic treatment for teeth with irreversible pulpitis or pulp necrosis.
• Avoiding dental trauma; using mouthguards during sports.
• Ensuring high-quality dental restorations to prevent leakage and secondary caries.

When to Seek Dental Care

It is important to seek dental care if you experience:

• Persistent toothache, especially if spontaneous, throbbing, or waking you at night.
• Pain when biting or chewing on a specific tooth.
• A tooth feeling "high" or "extruded."
• Swelling of the gums or face near a tooth.
• A pimple-like lesion (sinus tract opening) on the gums that may drain pus.
• Discoloration of a tooth, especially after trauma.
• Sensitivity to hot or cold that lingers after the stimulus is removed.

Early diagnosis and treatment of conditions leading to apical periodontitis provide the best chance of saving the tooth and preventing complications.