Acute Apical Periodontitis

Acute apical periodontitis (AP) is an inflammation of the periodontium that is primarily caused by an infection of the root canal system. The inflammation usually affects the alveolar bone, also known as the alveolar process, the periodontal ligament, and the cementum surrounding the apex of the tooth root (the periapical region).

Etiology

There are several possible reasons for AP:

• Microorganisms and toxins they produce in case of pulp infection resulting from caries or traumatic tissue exposure from cracks, fractures, or tooth attrition; decompensated periodontal disease; or a leaky temporary restoration. An infection can also occur during or after endodontic treatment if performed without a rubber dam.
• Physical factors: excessive instrumentation and overfilling of root canals, traumatic injury to periapical tissues, or tooth restoration in hyperocclusion.
• Chemical factors: irrigants, intracanal dressings, root canal filling materials, and devitalizing agents.

In the majority of cases, AP is caused by bacterial infection. Within the root canal system, bacteria can exist as planktonic organisms. However, most often, they form biofilms, which are aggregates of microorganisms attached to the dentin. For one thing, this mode of existence provides bacteria with effective protection against microbial competitors and the host immune system; for another, it makes them more resistant to a variety of antibacterial agents.

Pathogens usually enter the periapical tissues through the apical foramen, lateral canals, or root perforations. The bacteria found in untreated root canals are typically of a mixed type with approximately equal amounts of gram-positive and gram-negative species, dominated by obligate anaerobes. The most common bacterial pathogens include Fusobacterium, Dialister, Porphyromonas, Prevotella, Tannerella, Treponema, Pyramidobacter, Veillonella, Campylobacter, Parvimonas, Filifactor, Pseudoramibacter, Streptococcus, Propionibacterium, Olsenella, Actinomyces, Peptostreptococcus, and Eubacterium. Notably, evidence linking certain bacterial species to distinct AP symptoms is limited.

Acute (symptomatic) AP is a common consequence of total pulp necrosis. Nevertheless, it can also develop against viable, though inflamed, pulp tissue in the apical portion of the root canal. This may happen due to an infection of the vital pulp, resulting in the diffusion of inflammatory mediators, proinflammatory cytokines, chemokines, and bacterial toxins into the periapical region prior to complete pulp necrosis.

The pathophysiology of acute AP resembles that of a typical acute inflammatory response, involving vasodilation, increased vascular permeability, and the migration of leukocytes from the bloodstream into the perivascular space. These reactions lead to leukocyte infiltration, accumulation of immunoglobulins and plasma proteins, and complement activation in the damaged tissue.

In acute AP, the primary effector cells are polymorphonuclear neutrophils, which are known as the first line of defense against bacterial infection. Neutrophil death results in the release of lysosomal proteolytic enzymes, reactive oxygen species (such as nitric oxide), proinflammatory cytokines, eicosanoids, and matrix metalloproteinases, which further intensify the inflammatory response and contribute to tissue damage.

Although AP is predominantly an infectious disease, bacteria are typically found within the root canal system rather than in the periapical tissues.

Destruction of the apical bone is uncommon in AP. Since the condition is associated with a short-term acute inflammatory response, neutrophils and macrophages are not able to resorb bone tissue.

The possible outcomes of acute AP include:

• repair of periapical tissues (if the causative factor is eliminated by root canal treatment);
• abscess formation (in cases of extensive invasion of pyogenic bacteria);
• progression to chronic periapical inflammation (if the causative factor persists).

Anatomic Pathology

Depending on the underlying etiology, the following anatomical changes may be observed in the affected tooth:

• a deep carious lesion penetrating into the dental pulp;
• signs of compromised sealing in a restoration adjacent to the pulp tissues (e.g., defects, cracks, marginal pigmentation, or secondary caries);
• signs of trauma, such as cracks, dentin chipping, or pulp exposure.

The yellow-gray or gray-black pulp may be partially or completely necrotic. At the apex of the roots, the pulp may appear edematous, hyperemic, and bright red. The periodontal ligament space near the root apex is typically widened and filled with serous-hemorrhagic or purulent exudate.

Diagnosis

• Medical history: complaints regarding pain (its presence, location, intensity), duration of the condition, and any history of trauma or prior dental interventions.
• Visual examination: the dental crown may appear grayish due to the penetration of pulp breakdown products into the dentin tubules.
• Tooth percussion: usually painful.
•  Palpation along the mucobuccal fold: may also be painful, with edema and hyperemia of the mucosa observed in the projection of the root apex along the fold.
•  Pulp sensibility tests (thermal and electrical): no response to thermal or electrical stimuli.
• Radiography (intraoral contact radiography, radiovisiography, orthopantomography, or cone-beam computed tomography): may reveal a carious lesion, restoration, or traumatic defect penetrating into the pulp chamber, as well as the widening of the periodontal ligament space near the root apex.

Clinical Manifestations

Patients with acute AP often complain of prolonged, dull, localized pain that intensifies when biting on the affected tooth, along with a sensation that the tooth feels "raised" or higher than the adjacent teeth.

There may also be a noticeable change in tooth color. Past medical history may include a prolonged response to thermal stimuli and/or spontaneous pain that has subsided over time.

Treatment

The primary treatment for acute AP is endodontic therapy. This is when the necrotic pulp tissue is removed, followed by mechanical and chemical debridement of the root canals. If exudate is present in the canals, temporary intracanal dressings are recommended. Subsequently, the root canals are hermetically sealed, and the tooth is restored.

In cases where endodontic treatment may have unfavorable outcomes, tooth extraction is indicated.

For cases involving a restoration in hyperocclusion or mechanical trauma, occlusal adjustment by selective grinding may be performed, followed by regular monitoring.

Apical Abscess

An apical abscess, also known as a periapical abscess, is a purulent inflammation of the periapical tissues. It is typically triggered by a massive release of virulent bacteria from the root canal system.

Etiology

An acute apical abscess may initially arise from acute apical periodontitis (AP) or emerge as a complication of a pre-existing chronic inflammation in the periapical tissues.

The primary etiological factor is the invasion of pyogenic microorganisms that emerge into the inflamed periapical tissues from the root canal system, leading to extraradicular infection. The mixed microflora of an apical abscess is dominated by gram-negative anaerobic rods and Peptostreptococci. Polymorphonuclear neutrophils serve as the main effector cells in acute apical abscesses. Following phagocytosis and subsequent death of these cells, large amounts of tissue-destructive substances (e.g., hydrolases and oxygen radicals) are released. This damage exceeds the reparative capacity of macrophages, resulting in the destruction of the periodontal ligament and bone tissue in the periapical region. The osteoclast activity, accompanied by the recruitment of immune cells, leads to bone resorption in the affected area. The condition may also be aggravated by microorganisms that invade directly from the root canals and gradually destroy the tissues.

A chronic apical abscess, on the other hand, is characterized by a persistent focus of purulent inflammation, which drains through a fistula (an abnormal connection between two body parts). In such cases, the inflammatory process spreads to the spongy bone and one of the cortical plates, thus forming a fistula that allows continuous pus discharge.

The possible outcomes of an apical abscess include:

1. healing after the infection in the root canal has been eliminated (a necrotic pulp is removed and the abscess is drained);
2. progression to a chronic apical abscess with a fistula;
3. destruction of the cortical plate over an abscess that causes purulent exudate to spread into the subperiosteal space and suppurative odontogenic periostitis of the jaw develops;
4. spread of purulent inflammation through the fascial spaces of the head and neck.

Classification

Apical abscesses can be classified into the following types:

• an acute apical abscess;
• a chronic apical abscess with a fistula opening into the oral cavity;
• a chronic apical abscess with a fistula opening into the nasal cavity;
• a chronic apical abscess with a fistula opening into the maxillary sinus;
• a chronic apical abscess with a fistula opening onto the skin.

Anatomic Pathology

Depending on the etiology, the following anatomical changes may be observed in the affected tooth:

• a deep carious lesion penetrating into the dental pulp;
• signs of compromised sealing in a restoration adjacent to the pulp tissues (e.g., defects, cracks, marginal pigmentation, or secondary caries);
• signs of trauma, such as cracks, dentin chipping, or pulp exposure.

This condition is characterized by necrotic pulp that appears yellowish-gray or grayish-black. In cases of an acute apical abscess, a focus of destruction can be identified at the apex of the tooth, affecting the periodontal ligament and the alveolar bone. This area is filled with purulent exudate, surrounded by fibrovascular granulation tissue.

In chronic apical abscesses, the infection spreads to the spongy and compact bone, as well as the mucosa or skin, forming a fistula. The opening of a fistula typically presents as a raised, rounded soft tissue lesion with a hole in the center from which purulent exudate emerges. A fistula may develop near or at a distance from the infection site, e.g., on the vestibular or lingual surface of the mucosa of the alveolar process or on the attached gingiva. In some instances, it may run along the root of the tooth and open into the gingival sulcus or furcation area, forming a deep, narrow false pocket, which mimics a periodontal pocket or even a vertical root fracture. Additionally, a fistula may drain into the nasal cavity or maxillary sinus or open externally onto the skin of the face or neck.

The internal surface of a fistula tract may be partially or completely lined with epithelium, surrounded by inflamed connective tissue.

Diagnosis

• Medical history.
• Clinical examination: visual examination, percussion of the tooth, palpation along the mucobuccal fold, periodontal probing, and assessment of tooth mobility.
• Pulp sensibility tests (thermal and electrical).
• Radiography (intraoral contact radiography, radiovisiography, orthopantomography, or cone-beam computed tomography): a carious lesion, restoration, or traumatic defect penetrating into the pulp chamber may be revealed. A periapical radiolucency, indicating bone destruction, may appear as a round or irregularly shaped radiolucency around the root apex. A two-dimensional (2D) X-ray might only show a widened periodontal ligament space with no clear periapical radiolucency if the infection is confined to the spongy bone and the cortical plate remains intact.
• Fistula tract tracing: a gutta-percha point is inserted into the fistula opening until resistance is felt, followed by intraoral contact radiography. The method makes it possible to trace the origin of the infection.

Clinical Manifestations

Acute Apical Abscess

Patients typically present with localized pain in the affected tooth, which can be moderate to severe and intensifies when biting or chewing. There is often a sensation of pressure or a feeling that the tooth is "raised" or higher than the adjacent teeth. On visual examination, a tooth with a deep carious lesion, restoration, or traumatic defect penetrating the pulp chamber is observed. Percussion of the tooth elicits sharp pain, and the mucobuccal fold in the projection of the root apex may also be tender on palpation. If the cortical bone is involved, swelling and redness of the overlying mucosa may be noticed. Gingival probing depth remains within normal limits (1–3 mm), although slight tooth mobility may be present. There is usually no response to thermal or electrical pulp testing. Systemic symptoms, such as fever, submandibular or submental lymphadenopathy, and leukocytosis, may also be observed.

Chronic Apical Abscess

Patients with a chronic apical abscess may be asymptomatic or may report a small lesion or swelling on the gingiva. Visual examination reveals a tooth with a deep carious lesion, restoration, or traumatic defect penetrating the pulp chamber. Percussion of the tooth is typically painless or only mildly sensitive, and palpation of the mucobuccal fold is not usually tender. A fistula opening may be visible on the gingiva or skin, with purulent exudate draining from it. In cases where the fistula tract is blocked, localized soft tissue swelling may develop.

Treatment

The primary treatment for an apical abscess is endodontic therapy. This is when the necrotic pulp tissue or previous root canal filling material is removed, followed by mechanical and chemical debridement of the root canals. In cases with exudation from the root canals or a fistula, temporary intracanal dressings are recommended. Drainage of the purulent exudate may be achieved through the root canals or via the cortical bone adjacent to the affected area. Subsequently, the root canals are hermetically sealed, and the tooth is restored.

If access to the infection source is challenging, adjunctive microsurgical techniques may be employed. These may include periradicular curettage, root-end resection with retrograde filling, or root amputation.

Intentional replantation may also be considered.

In cases where endodontic treatment may have unfavorable outcomes, tooth extraction is indicated.

Apical Granuloma

Apical granuloma, or periapical granuloma, is the most common form of chronic apical periodontitis (AP). It is an inflammatory lesion composed of granulomatous tissue rich in lymphocytes, macrophages, and plasma cells.

Chronic AP is a long-term inflammatory process affecting the tissues around the root apex of the tooth. This condition leads to periapical bone resorption, which has no significant clinical symptoms but is detectable on radiography.

Etiology

Chronic inflammation in the periapical region is primarily triggered by a bacterial infection of the root canal system. In teeth that have not previously undergone endodontic treatment, AP serves as a protective response to the primary infection in the necrotic pulp. Another possible etiological factor is a secondary infection, introduced into the root canal system due to endodontic treatment (e.g., inadequate isolation during the procedure, improper obturation, or insufficient coronal sealing). Moreover, extrusion of chemical agents and root-filling materials beyond the apical foramen can lead to toxic tissue damage. Substances like talc, calcium salts, cellulose from paper points, or cotton fibers may promote the formation of a foreign body giant cell granuloma. Additionally, a foreign material in the periapical region may become a perfect substrate for a biofilm.

Types of microorganisms detected in teeth with AP:

• Primary infections: Dialister, Bacteroides, Pseudoramibacter, Porphyromonas, Treponema, Filifactor, Tannerella, Prevotella, Enterococcus, Veilonella, Olsenella, Pyramidobacter, Campylobacter, Propionibacterium, Streptococcus, Parvimonas, Fusobacterium, Eikenella, and Actinomyces.
• Previously treated teeth: Enterococcus faecalis (the most commonly identified species), Pseudoramibacter alactolyticus, Propionibacterium, Filifactor alocis, Dialister pneumosintes, Tannerella forsythia, Parvimonas micra, Prevotella intermedia, Treponema denticola, and Candida albicans.

The necrotic pulp within the root canal system provides an ideal environment for bacterial colonization and functioning. Here, bacterial aggregates are enclosed in an extracellular matrix and organized into biofilms that attach to the walls of the root canals. In this form, microorganisms are protected from the host immune system, as defense mechanisms cannot function effectively within the poorly vascularized root canal. Furthermore, the biofilm structure makes bacteria more resistant to a variety of antibacterial agents. If the biofilm in the root canal is not eradicated or substantially disrupted, AP may become chronic as the pathogens will persist. Histologically, macrophages and lymphocytes are the primary and predominant cells in this process, with occasional foam and giant cells observed.

The hallmarks of chronic AP are bone resorption in the periapical region and proliferation of fibrovacular granulation tissue. The former process is triggered by activated osteoclasts, while the latter represents an attempt to repair tissues and limit the inflammatory process. It is worth mentioning that resorption may also affect apical fragments of the tooth root.

The possible outcomes of apical granuloma include:

• healing of the periapical tissues following successful endodontic treatment;
• progression to an acute or chronic apical abscess if the source of infection persists and the host immune response is compromised by exposure to bacterial infection.

Anatomic Pathology

Depending on the etiology, the following anatomical changes may be observed in the affected tooth:

• a deep carious lesion penetrating into the dental pulp;
• signs of compromised sealing in a restoration adjacent to the pulp tissues (e.g., defects, cracks, marginal pigmentation, or secondary caries);
• signs of trauma, such as cracks, dentin chipping, or pulp exposure.

This condition is characterized by necrotic pulp that appears yellowish-gray or grayish-black. At the root apex, there is a focus of destruction of the periodontal ligament and bone, filled with granulomatous tissue. This tissue is infiltrated by mast cells, macrophages, lymphocytes, plasma cells, and occasionally polymorphonuclear leukocytes. In addition, multinucleated foreign body giant cells, foam cells, cholesterol crystals, and epithelial cells in the form of disorganized strands can be present. In the peripheral area, fibrous tissue is usually observed.

Diagnosis

• Medical history.
• Clinical examination: visual examination, percussion of the tooth, palpation along the mucobuccal fold, periodontal probing, and assessment of tooth mobility.
• Pulp sensibility tests (thermal and electrical).
• Radiography (intraoral contact radiography, radiovisiography, orthopantomography, or cone-beam computed tomography): a carious lesion, restoration, or traumatic defect penetrating into the pulp chamber may be revealed. A periapical radiolucency, indicating bone destruction, may appear as a round or irregularly shaped radiolucency with well-defined borders around the root apex. A two-dimensional (2D) X-ray might only show a widened periodontal ligament space with no clear periapical radiolucency if the cortical plate remains intact.

Currently, there are no noninvasive diagnostic methods capable of distinguishing a granuloma from a cyst. A definitive diagnosis can only be made based on biopsy results.

Clinical Manifestations

The condition is usually asymptomatic. On visual examination, a tooth with a deep carious lesion, restoration, or traumatic defect penetrating the pulp chamber is observed. Percussion of the tooth is typically painless, as is the palpation of the mucobuccal fold. However, if the cortical plate is involved, palpation may cause discomfort. There is usually no response to thermal or electrical pulp testing. Gingival probing depth remains within normal limits (1–3 mm), and the tooth mobility is physiological.

Treatment

Although radiography findings alone cannot differentiate this condition from other forms of AP and the histology is usually unknown, the main goal of treatment is to eliminate the underlying cause. For this purpose, endodontic therapy is performed. This is when the necrotic pulp tissue or previous root canal filling material is removed, followed by mechanical and chemical debridement of the root canals.

Subsequently, the root canals are hermetically sealed, and the tooth is restored. If access to the infection source is challenging, adjunctive microsurgical techniques may be employed. These may include periradicular curettage, root-end resection with retrograde filling, or root amputation. Intentional replantation may also be considered.

In cases where endodontic treatment may have unfavorable outcomes, tooth extraction is indicated.

Periapical Cyst

A periapical cyst is a pathological cavity in the area of the apex of the tooth root, containing fluid and lined with nonkeratinizing stratified squamous epithelium. It is considered one of the forms of chronic apical periodontitis (AP).

Etiology

The primary etiological factor of periapical cysts is a bacterial infection of the root canal system. Chronic inflammatory cells are the main driver behind such lesions. Epithelial cell rests of Malassez can also contribute to the condition. These cells are remnants of the Hertwig's epithelial root sheath during tooth development and can be considered as unipotent stem cells.

During an inflammatory reaction in periapical tissues, growth factors and cytokines are released, leading to the proliferation of epithelial cell rests of Malassez.

The exact causes of apical cysts are unknown. However, there are several theories that attempt to explain their origin:

• Nutrient deficiency theory: as the epithelial rests grow, their central cells move further away from the nutrient source, resulting in necrosis. The accumulation of tissue breakdown products attracts granulocytes and neutrophils to the necrosis zone, forming microcavities. These microcavities eventually merge to form a cystic cavity, which is lined with nonkeratinizing stratified squamous epithelium.
• Abscess theory: when an abscess forms in connective tissue, epithelial cells proliferate and line the abscess cavity due to their tendency to cover the exposed surface of connective tissue.
• Epithelial strand fusion theory (inflammatory hyperplasia): epithelial tissue, in the form of disorganized strands within an apical granuloma, proliferates and merges to create a three-dimensional spherical structure made of fibrovascular connective tissue containing inflammatory cells. As blood supply becomes insufficient, tissues start to degrade, and a cystic cavity forms. The cystic fluid originates from the capillary network of the granuloma through processes of transudation and exudation of plasma (the liquid component of blood), as well as the breakdown of formed elements of blood.

The epithelial cells lining the cystic cavity cannot proliferate independently if not stimulated by cytokines or growth factors.

Over time, these cysts may slowly enlarge, likely due to degradation of the fibrous connective tissue capsule (induced by matrix metalloproteinases) and resorption of the surrounding bone. Subsequently, inflammatory mediators and cytokines stimulate proliferation of epithelial cells and mediate bone resorption in areas of AP. Furthermore, bone-resorbing factors may be secreted by epithelial cell rests of Malassez, which may exacerbate the condition.

As the cyst expands, it can put pressure on surrounding structures, potentially displacing the roots of the adjacent teeth and causing external resorption. It may also deform the maxillary sinus wall or even erode it, eventually invading the sinus itself. If left untreated, periapical cysts can destroy significant portions of the adjacent bone tissue. In advanced cases, the process may extend to the body and ramus of the mandible, resulting in a pathological fracture of the jaw. Over time, the cyst may become abscessed.

Classification

• Periapical true cyst: the lumen is completely enclosed by the epithelial lining and has no connection with the root canal.
• Periapical pocket cyst (bay cyst, pouch-like cyst): the lumen connects with the root canal of the affected tooth.

Anatomic Pathology

The following anatomical changes may be observed in the affected tooth:

• a deep carious lesion penetrating into the dental pulp;
• a failed tooth restoration in close proximity to the pulp tissues;
• signs of trauma, such as cracks, dentin chipping, or pulp exposure.

This condition is characterized by necrotic pulp that appears yellowish-gray or grayish-black. In the periapical region, there is a focus of destruction of the periodontal ligament and bone. A round or oval periapical cyst is typically located at the root apex and has the following structure:

1. Connective tissue capsule: contains all cells found in apical granulomas.
2. Epithelial lining: represented by hyperplastic, nonkeratinizing stratified squamous epithelium. It may be continuous or intermittent; some areas may bear no lining at all. In some cases, the lining may consist of ciliated epithelium. Both the lining and the connective tissue capsule are often infiltrated with inflammatory cells.
3. Cystic cavity (lumen): filled with a straw-colored opalescent fluid, which may contain inflammatory exudate, cholesterol crystals, necrotic epithelial cells, remnants of resorbed bone, or bacterial colonies.

Diagnosis

• Medical history.
• Clinical examination: visual examination, percussion, and palpation along the mucobuccal fold.
• Pulp sensibility tests (thermal and electrical).
• Radiography (intraoral contact radiography, radiovisiography, orthopantomography, or cone-beam computed tomography): may reveal a carious lesion, restoration, or traumatic defect penetrating into the pulp chamber. A periapical radiolucency, indicating bone destruction, may appear as a round or oval radiolucency with well-defined borders around the root apex. In some cases, a radiopaque rim may be seen at the periphery. Roots adjacent to the lesion may be displaced or shortened.

Currently, there are no noninvasive diagnostic methods capable of distinguishing a granuloma from a cyst. The radiolucency size at the root apex can only provide indirect evidence: if it measures between 10 and 20 mm, there is a 60 % likelihood of a cyst; if it exceeds 200 mm², the chances increase up to 100 %. However, a definitive diagnosis can only be made based on the results of a surgical biopsy or tooth extraction.

Clinical Manifestations

Typically, the affected tooth is asymptomatic. Most often, cysts are incidental findings during radiography. Patients may complain of swelling on the vestibular or palatal surface of the lower or upper jaw (the mandible and maxilla, respectively). On visual examination, a tooth with a deep carious lesion, restoration, or traumatic defect penetrating the pulp chamber is observed. Percussion of the tooth is painless, as is the palpation of the mucobuccal fold.

There may be a jaw swelling of a hemispherical shape, firm and painless on palpation, with no changes in the overlying mucosa. If the cortical plate in the affected area is thinned, bone crepitus may be felt on palpation of the protrusion. If the cortical plate is destroyed, palpation at the apex of the affected tooth may reveal fluctuation. In cases where the cyst is located in the area of the upper incisors, bulging of the floor of the nasal cavity (Gerber’s ridge) may be observed.

The affected tooth typically does not respond to thermal or electrical stimuli, which is a key diagnostic criterion, especially in cases with radiographic evidence of radiolucency in the periapical region of multiple teeth.

Treatment

There is currently no definitive evidence to confirm whether periapical cysts can regress following nonsurgical endodontic treatment. Considering the proposed mechanisms of pathogenesis, epithelial growth may cease once the stimulating bacterial factor is eliminated, for example, after endodontic treatment. Subsequently, the epithelial lining may become thin or disappear, providing the necessary conditions for healing.

Therefore, the first step to treat this cyst type is endodontic therapy. This is when the necrotic pulp tissue or previous root canal filling material is removed, followed by mechanical and chemical debridement of the root canals. If indicated, intracanal cyst aspiration may be performed during canal instrumentation. Subsequently, the root canals are hermetically sealed, and the tooth is restored.

For larger cysts (over 3 cm), decompression may be indicated. This can be achieved in several ways. The first technique aims to reduce the cyst size by making a surgical incision in the cyst wall and draining the fluid inside. According to another technique, the cyst contents should be aspirated extracanally, and the cavity is then irrigated with sterile saline using two separate large-gauge needles.

Later on, if the periapical lesion does not heal, enucleation of the cyst may be required. It can be performed through periapical curettage, root-end resection with retrograde filling, or root amputation with simultaneous removal of the cyst membranes.

In cases where endodontic treatment or periapical surgery may have unfavorable outcomes, tooth extraction is indicated.

Condensing Osteitis

Condensing osteitis, also known as focal sclerosing osteomyelitis or focal sclerosing osteitis, is a localized area of increased bone formation around the apex of the tooth root. This condition typically develops in response to a prolonged bacterial stimulus.

Etiology

It is believed that condensing osteitis arises from a long-term, low-grade inflammatory process. This inflammation is usually triggered by low-virulence microorganisms in the root canal system associated with irreversible pulpitis, pulp necrosis, or chronic AP. Instead of bone resorption, the condition stimulates osteoblasts through growth factors or cytokines, leading to proliferation of trabecular or spongy bone around the root apex.

Condensing osteitis is more common in children and young adults. In these age groups, it tends to affect the area of premolars and molars of the lower jaw, though it can occur in other teeth as well.

The outcome of condensing osteitis is healing of tissues following successful endodontic treatment; sometimes the excess bone remodels back to a normal state.

Anatomic Pathology

The lesion is usually located around the root apices of the mandibular molars or premolars.

The following anatomical changes may be observed in the affected tooth:

• a deep carious lesion penetrating into the dental pulp;
• a restoration in close proximity to the pulp chamber or directly adjacent to the pulp tissues;
• signs of compromised sealing in a restoration (e.g., defects, cracks, marginal pigmentation, or secondary caries);
• signs of trauma, such as cracks, dentin chipping, or pulp exposure.

The pulp may appear as dense, whitish fibrous scar tissue or as yellowish-gray or grayish-black necrotic tissue. The periodontal ligament space may be widened. In the periapical region, concentric bone deposition occurs; however, no bone resorption is observed. The newly formed bone tissue is infiltrated by a small number of lymphocytes.

As the bone marrow spaces become smaller and obliterated, the tissue resembles compact bone, showing fewer lacunae, many of which lack osteocytes.

Diagnosis

• Medical history.
• Clinical examination: visual examination, percussion, and palpation along the mucobuccal fold.
• Pulp sensibility tests (thermal and electrical).
• Radiography (intraoral contact radiography, radiovisiography, orthopantomography, or cone-beam computed tomography): a carious lesion, restoration, or traumatic defect penetrating into the pulp chamber, as well as the widening of the periodontal ligament space may be revealed. In the root apex region, there may be a well-defined or poorly visible concentrically arranged radiopaque mass without a radiolucent rim. The compact bone around the root apex is typically intact.

Clinical Manifestations

The condition is usually asymptomatic. However, some patients may report symptoms typical of chronic irreversible pulpitis, such as prolonged pain triggered by thermal or chemical stimuli. Depending on the cause, a deep carious lesion, restoration, or traumatic defect penetrating the pulp chamber may be apparent. Percussion of the tooth is typically painless, as is the palpation of the mucobuccal fold. Thermal testing may be positive if the vital pulp is in a state of irreversible inflammation. No response means that the pulp has necrotized. The affected tooth usually does not respond to electrical pulp testing, or it may show a higher threshold for electrical stimulation compared to that of healthy teeth.

Treatment

The primary treatment for condensing osteitis is endodontic therapy. This is when the necrotic pulp tissue is removed, followed by mechanical and chemical debridement of the root canals. Subsequently, the canals are hermetically sealed, and the tooth is restored.

In cases where endodontic treatment may have unfavorable outcomes, tooth extraction is indicated.

Antibiotic prophylaxis during nonsurgical and surgical endodontic treatment is recommended for the following patient groups:

• patients receiving intravenous bisphosphonate therapy (in cases of periapical surgery);
• patients at risk of infective endocarditis (e.g., complex congenital heart disease, prosthetic heart valves, history of infective endocarditis);
• patients with immunodeficiencies (e.g., leukemia, HIV/AIDS, end-stage renal disease and dialysis, inherited immunodeficiency disorders, uncontrolled diabetes mellitus, as well as immunodeficiencies caused by chemotherapy and post-transplant immunosuppressive or steroid medications);
• patients who have undergone joint replacement within the first three months after surgery;
• patients undergoing cranial radiotherapy.