(Cohen)
Acute Apical Abscess
This condition is defined as an inflammatory reaction to pulpal infection and necrosis characterized by rapid onset,
spontaneous pain, tenderness of the tooth to pressure, pus formation, and swelling of associated tissues.6 A tooth with an
acute apical abscess will be acutely painful to biting pressure, percussion, and palpation. This tooth will not respond to
any pulp vitality tests and will exhibit varying degrees of mobility. The radiograph or image can exhibit anything from a
widened periodontal ligament space to an apical radiolucency. Swelling will be present intraorally and the facial tissues
adjacent to the tooth will almost always present with some degree of swelling. The patient will frequently be febrile, and
the cervical and submandibular lymph nodes may exhibit tenderness to palpation.
Chronic Apical Abscess
This condition is defined as an inflammatory reaction to pulpal infection and necrosis characterized by gradual onset, little
or no discomfort, and the intermittent discharge of pus through an associated sinus tract.6 In general, a tooth with a chronic
apical abscess will not present with clinical symptoms. The tooth will not respond to pulp vitality tests, and the radiograph
or image will exhibit an apical radiolucency. Usually the tooth is not sensitive to biting pressure but can “feel different” to
the patient on percussion. This entity is distinguished from asymptomatic apical periodontitis because it will exhibit
intermittent drainage through an associated sinus tract.
(nisha garg)
ACUTE APICAL ABSCESS
It is a localized collection of pus in the alveolar bone at the rootmapex of the tooth, following the death of pulp with
extension of the infection through the apical foramen into periradicular tissue (Fig. 3.41).
Etiology
• Most common cause is invasion of bacteria from necrotic pulp tissue.
• Trauma, chemical or any mechanical injury resulting in pulp necrosis.
• Irritation of periapical tissue by chemical or mechanical treatment during root canal treatment.
Tissue at surface of swelling appears taut and inflamed and pus starts to form underneath it. Surface tissue may become
inflated from the pressure of underlying pus and finally rupture from this pressure. Initially, the pus comes out in the form
of a small opening but latter it may increase in size or number depending upon the amount of pressure of pus and softness
of the tissue overlying it. This process is beginning of chronic abscess.
Pathophysiology of Apical Abscess Formation
Increase in pulpal pressure
↓
Collapse of venous circulation
↓
Hypoxia and anoxia of local tissue
↓
Localized destruction of pulp tissue
↓
Formation of pulpal abscess because of breakdown of PMNs, bacteria and lysis of pulp remnants
Features of Acute Apical Abscess
• Tooth is nonvital
• Pain
– Rapid onset
– Readily localized as tooth becomes increasingly tender to percussion
– Slight tenderness to intense throbbing pain
– Marked pain to biting
• Swelling
– Palpable, fluctuant
– Localized sense of fullness
• Mobility
– May or may not be present
• Tooth may be in hyperocclusion
• Radiographic changes
– No change to large periapical radiolucency
Symptoms
• In early stage, there is tenderness of tooth which is relieved by continued slight pressure on extruded tooth to push it back
into alveolus.
• Later on, throbbing pain develops with diffuse swelling of overlying tissue.
• Tooth becomes more painful, elongated and mobile as infection increases in later stages.
• Patient may have systemic symptoms like fever, increased WBC count.
• Spread of lesion towards a surface may take place causing erosion of cortical bone or it may diffuse and spread widely
leading to formation of cellulitis (Fig. 3.42). Location of swelling is determined by relation of apex of involved tooth to
adjacent muscle attachment (Fig. 3.43).
Diagnosis
• Clinical examination.
• In initial stages, locating a tooth is difficult due to diffuse pain. Location of the offending tooth becomes easier when
tooth gets slightly extruded from the socket.
• Pulp vitality tests give negative response.
• Tenderness on percussion and palpation.
• Tooth may be slightly mobile and extruded from its socket.
• Radiography helpful in determining the affected tooth as it may show caries or evidence of bone destruction at root apex.
Histopathology
Polymorphonuclear leukocytes infiltrate and initiate inflammatory response
↓
Accumulation of inflammatory exudates in response to active infection
↓
Distention of periodontal ligament
↓
Extrusion of the tooth
↓
If the process continues, separation of periodontal ligament
↓
Tooth becomes mobile
↓
Bone resorption at apex
↓
Localized lesion of liquefaction necrosis containing polymorphonuclear leukocytes, debris, cell remnants and purulent
exudates
Management of an Acute Apical Abscess
• Drainage of the abscess should be initiated as early as possible. This may include:
a. Nonsurgical endodontic treatment (Root canal therapy)
(Fig. 3.44)
b. Incision and drainage
c. Extraction
Considerations regarding the treatment of a tooth with periapical abscess depend on following factors:
• Prognosis of the tooth
• Patient preference
• Strategic value of the tooth
• Economic status of the patient
• In case of localized infections, systemic antibiotics provide no additional benefit over drainage of the abscess
• In the case of systemic complications such as fever, lymphadenopathy, cellulitis or patient who is immunocompromised,
antibiotics should be given in addition to drainage of the tooth
• Relieve the tooth out of occlusion in hyperocclusion cases
• To control postoperative pain following endodontic therapy, nonsteroidal anti-inflammatory drugs should be given.
Torabinejad
Acute Apical Abscess
Etiology
Acute apical abscess (AAA) is a localized (Figure 4-22, A) or diffuse (Figure 4-22, B) liquefaction lesion of pulpal origin that
destroys periradicular tissues and a severe infl ammatory response to microbial and nonbacterial irritants from a necrotic pulp.
Signs and Symptoms
AAA is characterized by rapid onset and spontaneous pain. Depending on the severity of the reaction, patients with AAA usually
have moderate to severe discomfort and/or swelling. There often is no swelling if the abscess is confi ned to bone. In addition,
they occasionally have systemic manifestations of an infective process such as elevated temperature, malaise, and leukocytosis.
Because these fi ndings are only observed in association with a necrotic pulp, electrical or thermal stimulation produces no
response. However, these teeth are usually painful to percussion and palpation. Depending on the degree of hard tissue
destruction infl icted by irritants, radiographic features of AAA range from no changes to widening of the PDL space to an
obvious radiolucent lesion.
Histologic Features
Histologic examination of AAA usually shows a localized destructive lesion of liquefaction necrosis containing numerous
disintegrating PMN leukocytes, debris and cell remnants, and an accumulation of purulent exudate (Figure 4-22, C). Surrounding
the abscess is granulomatous tissue; therefore the lesion is best categorized as an abscess within a granuloma. Notably, the
abscess often does not communicate directly with the apical foramen; frequently an abscess will not drain through an accessed
tooth. Removal of the underlying cause, release of pressure (drainage where possible), and routine root canal treatment will lead
to resolution of most cases of AAA.
Chronic Apical Abscess
The chronic apical abscess (CAA) is an inflammatory lesion of pulpal origin that is characterized by the presence of a long-
standing lesion that has resulted in an abscess that is draining to a mucosal (sinus tract) or skin surface.
Etiology
CAA has a pathogenesis similar to that of AAA. It also results from pulpal necrosis and is usually associated with chronic apical
periodontitis that has formed an abscess. The abscess has “burrowed” through bone and soft tissue to form a sinus tract stoma on
the oral mucosa (Figure 4-23, A) or sometimes onto the facial dermis. The histologic findings in these lesions are similar to those
found in SAP (Figure 4-23, B). CAA may also drain through the periodontium into the sulcus and may mimic a periodontal
abscess or pocket (see Chapter 7).
Signs and Symptoms
Because drainage exists, CAA is usually asymptomatic, except when there is occasional closure of the sinus pathway, which can
cause pain. Clinical, radiographic, and histopathologic features of CAA are similar to those described for AAP. An additional
feature is the sinus tract, which may be lined partially or completely by epithelium surrounded by infl amed connective tissue.68