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ACUTE PERIAPICAL ABSCESS

(Synonyms: Acute abscess, acute apical abscess acute dentoalveolar abscess, acute

periapical abscess, acute radicular abscess)

Apical periodontitis is an inflammatory disease affecting the tissues surrounding the root

end of a tooth and is caused by root canal (endodontic) infection. The disease can

manifest itself in different clinical ways, including the development of an acute abscess.

A recurrent theme in this regard is the association of certain bacterial species with clinical

signs and symptoms. However, the search for a single or even a small group of species

to be considered the major pathogen involved with acute endodontic infections has

proven fruitless65. Recent studies in the fields of molecular and cellular microbiology and

immunology have provided information to implicate a multitude of factors in the

pathogenesis of symptomatic apical periodontitis, including its most severe form, the

acute apical abscess.

Definition :

Localized collection of pus in the alveolar bone at root apex of tooth following death

of pulp, with extension of infection through apical foramen in to periradicular tissue .

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THE DISEASE PROCESS

An abscess consists of a collection of pus into a cavity formed by tissue liquefaction. The

terms dental abscess, dentoalveolar abscess, and odontogenic abscess are often used

synonymously to describe abscesses formed in the tissues around the tooth. The cause

may be an endodontic infection (acute apical abscess) or a periodontal infection

(periodontal abscess and pericoronitis).

Endodontic infection develops only in root canals of teeth devoid of a vital pulp. This may

be due to necrosis of the dental pulp as a consequence of caries or trauma to the tooth

or to removal of the pulp tissue for previous root canal treatment. Once the infection is

established in the root canal, bacteria may contact the periradicular tissues via apical and

lateral foramina or root perforations and induce a chronic or acute inflammatory response
66.

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The chronic response is usually asymptomatic and almost invariably leads to bone

resorption around the root apex, which is the typical radiographic feature of apical

periodontitis. Acute periradicular inflammation in turn usually gives rise to signs and

symptoms, including pain and swelling. The acute (symptomatic) process may develop

without previous chronic inflammation or may be the result of exacerbation of a previously

chronic asymptomatic lesion. It has been estimated that the incidence of exacerbations

of apical periodontitis (i.e., asymptomatic lesions becoming symptomatic) is about 5% per

year.

The acute abscess can be regarded as an advanced stage of the symptomatic form of

apical periodontitis. In acute endodontic infections, not only are the involved bacteria

located in the root canal, but they invade the periradicular tissues and have the potential

to spread to other anatomical spaces of head and neck to form a cellulitis or phlegmon,

which is a disseminating diffuse inflammatory process with pus formation.

The purulent exudate formed in response to root canal infection spreads through the

medullary bone to perforate the cortical bone and discharge into the submucous or

subcutaneous soft tissue. In many cases, swelling develops only intraorally . In the

maxilla, acute apical abscesses drain through the buccal or palatal bone into the oral

cavity or occasionally into the maxillary sinus or the nasal cavity. Apical abscesses of

mandibular teeth may drain through the buccal or lingual bone into the oral cavity.

However, the infectious process may also extend into fascial spaces of the head and neck

and result in cellulitis and systemic signs and symptoms, with consequent complications

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Etiology:

Due to bacterial invasion of dead pulp tissue. It may also be caused due to trauma,

chemical or mechanical irritation. Because the pulp is enclosed chamber drainage is not

possible and infection continue to extend through least resistant path i.e.,. apical foramen

and thereby involving periodontal ligament and periradicular bone.

Symptoms :

o First symptom is tenderness that can be relieved by continued slight

pressure on the extruded tooth to push it back to alveolus. Later

patient has severe throbbing pain with small swelling on the soft

tissue overlying. As infection proceed swelling become more

pronounced beyond orginal site. If untreated infection may progress

to osteotis, periostitis, cellulitis and osteomyelitis.

o The contained pus may break through to form sinus tract to open to

labial or buccal mucosa.

o Swelling is usually seen in the adjacent tissue close to affected tooth,

when it become extensive the resultant cellulites occurs. When

maxillary anterior teeth is involved particularly cuspid, swelling of

upper lip may extend to both eyelids.

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o When maxillary posterior teeth is affected the check may swell to

immense size distorting facial features.

o In mandibular posterior teeth the swelling extend to or even around

border of jaw into submaxillary region tissue and the surface of

swelling become taunt or inflamed pus starts to form beneath.

Continued liquefaction causes pressure of underlying pus and finally causes

rupture. Pus extend from tiny opening and become large further or may have 2 or more

opening depending a degree of softening of tissue and the pressure exterted.

A gutta-percha is placed on the sinus tract and assessed radiographically points to

involved tooth. Point at which pus breaks in to mouth depends upon thickness of alveolar

bone and overlying soft tissue. Usually confined pus take path of least resistance in upper

jaw.

In addition to localized symptom a general systemic reaction occurs patient

may appear pale irritable and weakened from pain and loss of sleep and

from absorption of septic products.

Diagnosis :

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Is from clinical examination and subjective history. In early stage it is difficult to locate

tooth. Once infection is progressed to the process of periodontitis and extrusion a

radiographic evaluation show thickening of periodontal ligament space evidence of

breakdown of bone or region of root apex.

Diagnosis is made by electric test. Pulp testing of affected pulp is necrotic and does

not respond to electric pulp testing or application of cold. Tooth is tender on

percussion, apical mucosa is tender palpation, and tooth may be mobile and extruded.

Complications Stemming from Acute Apical Abscesses

Almost 60% of all non-traumatic dental emergencies are associated with acute apical

abscesses and toothaches. Acute dental abscesses have been reported to cause severe

complications and even mortality.

Mortality is more likely a result of sepsis or airway obstruction, but death due to a

spreading infection leading to massive hemorrhage from the subclavian vein into the

pleural cavity has been reported The spread of bacteria from endodontic abscesses to

other tissues may give rise to fascial plane infections The most commonly affected fascial

spaces are the sublingual, submandibular, buccal and pterygomandibular spaces, but

others such as the temporal, masseteric, lateral pharyngeal, and retropharyngeal spaces

can be occasionally involved.

The spread of infections of endodontic origin into the fascial spaces of the head and neck

is determined by the location of the root end of the involved tooth in relation to its overlying

buccal or lingual cortical plate, the thickness of the overlying bone, and the relationship

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of the apex to the attachment of a muscle. For example, if a mandibular molar is affected

and its root apices lie closer to the lingual cortical plate and above the attachment of the

mylohyoid muscle, the purulent exudate can break through the lingual cortical plate into

the sublingual space. If the root apices instead lie below the attachment of the mylohyoid

muscle, the infection can spread into the submandibular space. If infection affects the

sublingual and submandibular spaces bilaterally as well as the submental space, a

condition known as Ludwig’s angina.

Another example of abscess complications involves infections of the midface, which can

be very dangerous and result in cavernous sinus thrombosis. This is also a life-

threatening infection, in which a thrombus formed in the cavernous sinus breaks free and

leads to spread of the infection. Under normal conditions, the angular and ophthalmic

veins and the pterygoid plexus of veins flow into the facial and external jugular veins. If

an infection has spread into the midfacial area, however, edema and the resultant

increased pressure cause the blood to back up into the cavernous sinus. Once in the

sinus, the blood can stagnate and clot. The resultant infected thrombi remain in the

cavernous sinus or escape into the circulation.

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Other reported complications of disseminating dental infections include brain abscess

septicemia in a patient with multiple myeloma, deep neck infection mediastinitis

necrotizing fasciitis , orbital abscess and cervical spondylodiscitis with spinal epidural

abscess . It has been suggested that some host-related factors may contribute toward

increased morbidity and mortality associated with acute dental abscesses, including

diabetes, chronic alcohol and tobacco consumption, malnourishment, and the use of illicit

substances

Differential diagnosis:

Periodontal abscess and irreversible pulpitis.

Periodontal abscess is accumulation of pus along root surface of tooth that originates

from infection in supporting structure of tooth. Associated with periodontal pocket and

manifest by slight pain or pressure pus may exudate through the sulcus. Swelling is

present opposite to midsection of root and gingival border.

Prognosis:

Is favorable and depend upon degree of local involvement and tissue destruction. Pain

can be relieved with adequate drainage. Tooth can be saved by endodontic treatment. In

severe case combined periodontal and endodontic treatment is done.

Microbial Diversity in Acute Apical Abscesses

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Samples for microbiological analyses of abscesses can be taken either from the root

canals of affected teeth or by aspiration of the purulent exudate from the swollen

mucosa/skin. Culture and molecular microbiology studies have clearly demonstrated that

the apical abscess microbiota is mixed and conspicuously dominated by anaerobic

bacteria provides a compilation of the main microbiological findings from most of these

studies. It is noteworthy that while some bacterial species or groups are reported in many

studies, the most prevalent species vary from study to study.

At a broader taxonomic level, the large majority of the frequently detected bacterial

species belong to seven different bacterial phyla, namely, the Firmicutes (e.g., genera

Streptococcus, Dialister,Filifactor, and Pseudoramibacter), Bacteroidetes(e.g., genera

Porphyromonas, Prevotella, and Tannerella), Fusobacteria (e.g., genera Fusobacterium

and Leptotrichia), Actinobacteria (e.g.,genera Actinomyces and Propionibacterium),

Spirochaetes (e.g., genus Treponema), Synergistetes (e.g., genus Pyramidobacter and

some as-yet-uncultivated phylotypes), and Proteobacteria (e.g.,genera Campylobacter

and Eikenella) 67.

Histopathology:
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Marked infiltration of PMNL and rapid accumulation of inflammatory exudate in response

to active infection. Also some mononuclear cells are found, the chief inflammatory cells

are PMNL. As more PMNL cells die pus is formed root canal is devoid of tissue and

clumps of micro org are seen 41.

Treatment:

Treatment of acute apical abscesses involves incision for drainage and root canal

treatment or extraction of the involved tooth to remove the source of infection. In some

cases, drainage can be obtained through the root canal, but when swelling is present,

incision for drainage should also be performed whenever possible, since this approach

has been shown to produce a quicker improvement than drainage only by opening of the

root canal.

 Adjunctive systemic antibiotics are not necessary in most cases of localized and

uncomplicated apical abscesses, Analgesics may be prescribed for pain control.

 The selective occasions when antibiotics are indicated in cases of acute apical

abscesses include the following: abscesses associated with systemic involvement,

including fever, malaise, and lymphadenopathy; disseminating infections resulting

in cellulitis, progressive diffuse swelling, and/or trismus; and abscesses in

medically compromised patients who are at increased risk of a secondary (focal)

infection following bacteremia.

 The selective occasions when antibiotics are indicated in cases of acute apical

abscesses include the following: abscesses associated with systemic involvement,

including fever, malaise, and lymphadenopathy; disseminating infections resulting

in cellulitis progressive diffuse swelling, and/or trismus; and abscesses in medically

compromised patients who are at increased risk of a secondary (focal) infection

following bacteremia.

The selection of antibiotics in clinical practice is either empirical or based on the results

of microbial susceptibility testing. For diseases with known microbial causes for which the

probable microbiota has been established in the literature, empirical therapy may be

used. This is especially applicable to acute dental abscesses because culture-dependent

antimicrobial tests of anaerobic bacteria can take too long to provide results about

antibiotic susceptibility (around 7 to 14 days). Therefore, it is preferable to opt for an

antimicrobial agent whose spectrum of action includes the most commonly detected

bacteria.

Most of the bacterial species involved with endodontic infections, including abscesses,

are susceptible to penicillin.This makes these drugs the first choice for treatment of

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endodontic infections when allergy of the patient to penicillin has been ruled out. Penicillin

V or amoxicillin has been commonly prescribed.

In addition, amoxicillin may provide more rapid improvement in pain or swelling, and

patient compliance with the prescribed regimen may be better because of the longer

dosage interval of amoxicillin . In even more serious cases, including life-threatening

conditions, association of amoxicillin with either clavulanic acid or metronidazole may be

required to achieve optimum antimicrobial effects as a result of the spectrum of action

being extended to include penicillin-resistant strains,

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