ABSCESS OF THE PERIODONTIUMPRESENTED BY SHILPA SHIVANANDII MDS

ContentsIntroductionAbscess of the periodontiumPeriodontal abscessDefinitionPrevalenceClassificationEtiologyClinical features

Pathogenesis and histopathologyMicrobiologyDiagnosis Differential Diagnosis Treatment Complications and postoperative care.

Gingival abscessPericoronal abscessConclusion References

INTRODUCTION

Abscess- Localised collection of pus purulent material collected in a cavity caused by destruction of tissues. (GPT)Abscesses of the periodontium have been classified primarily, based on their anatomical locations in the periodontal tissue. There are three types: Gingival abscessPericoronal abscessPeriodontal abscess.

Among all the abscesses of the periodontium, the periodontal abscess is the most important one, which often represents the chronic and refractory form of the disease.

It is a destructive process occurring in the periodontium, resulting in localized collections of pus, communicating with the oral cavity through the gingival sulcus or other periodontal sites and not arising from the tooth pulp

Periodontal Abscess

A localized purulent infection within the tissues adjacent to the periodontal pocket that may lead to the destruction of periodontal ligament and alveolar bone

DEFINITIONA periodontal abscess is a localized

purulent infection in the periodontal tissue (GLICKMAN)

A localized purulent inflammation of the periodontal tissues. It is also known as Lateral periodontal abscess or Parietal Abscess.

(AAP GLOSSARY 1992)

An acute, destructive process in the periodontium resulting in localized collection of pus communicating with the oral cavity through the gingival sulcus or other periodontal sites & not arising from the tooth pulp.

(RANNY 1977)

A lesion with an expressed periodontal break down occurring during a limited period of time & with easily detectable clinical symptoms with a localized accumulation of pus located within the gingival wall of the periodontal pocket.

(Hafstrom et al-1994, Dewitt et al1985)

CLASSIFICATIONI) Depending on the location of the abscess (Gillette and Van House-1980, AhI et al 1986)Gingival Abscess localized painful swelling affecting only the marginal and interdental gingiva Mainly due to impaction of foreign objects May be present on a previously healthy gingiva Periodontal Abscess with similar symptoms, usually affect deeper periodontal structures, including deep pockets, furcations and vertical osseous defects. usually located beyond Mucogingival junction.

II) Depending on the course of the lesion (Galego-Feul et al-1995, Carranza - 1990) Acute periodontal abscess. Presents with symptoms like pain, tenderness, sensitivity to palpation and suppuration upon gentle pressure. Chronic periodontal abscess. Normally associated with a sinus tract. Usually asymptomatic, can refer mild symptoms

III. Depending on the number (Topell et al 1990) Single periodontal abscess related to local factors, which contribute to the closure of the drainage of a periodontal pocket. Multiple periodontal abscess Seen in uncontrolled diabetes mellitus, medically compromised patients, in patients with untreated periodontitis after systemic antibiotic therapy for non-oral reasons .

IV. According to periodontal tissue affected (Meng -1999)Gingival abscess - in previously healthy sites and caused by impaction of foreign bodies. Periodontal abscess either acute or chronic developing into a periodontal pocket. Pericoronal abscess in incompletely erupted teeth.

Depending on the cause of acute infectious process (Lindhe) Periodontitis related abscess: - when the acute infection originates from biofilm present in a deepened periodontal pocket. Non-periodontitis related abscess: - when the acute infection originates from other local source, such as foreign body impaction or alteration in root integrity.

VI. Based on location of abscess (Carranza)Abscess in the supporting periodontal tissues along the lateral aspect of the root, sinus tract present.

Abscess in the soft tissue wall of a deep periodontal pocket.

PREVALENCE 3rd most prevalent emergency infection, after acute alveolar (14-25%) and periodontitis (10-11%).

More likely to occur in a pre-existing periodontal pocket.

More in molar sites (> 50%)

The prevalence of periodontal abscesses has been studied in emergency dental clinics (Galego-Feal et al. 1996, Ahl et al. 1986) In general dental clinics (Lewis et al. 1990)In periodontitis patients before and during periodontal treatment (Gray et al. 1994) andIn periodontitis patients during periodontal maintenance

Gray et al (1994) monitored periodontal patients in an army clinic and found that periodontal abscess had prevalence of 27.5%. In this population, 13.5% of patients undergoing active periodontal treatment had abscess formation and while in untreated patients it is 59.7%.

Kaldahl et al (1996) in a 7-year prospective longitudinal treatment study for occurrence of periodontal abscess. From the 51 patients included, 27 developed abscesses were detected.

16 out of the 27 abscess sites had an initial probing pocket depth greater than 6 mm, and in about 8 sites the periodontal probing depth was 5-6 mm.

ETIOLOGY Periodontal abscesses have been either directly associated to periodontitis or to sites without the prior existence of a periodontal pocket.

Periodontal abscesses in periodontitis (Periodontitis Related Abscess) In periodontitis, a periodontal abscess represents a period of active bone destruction (exacerbation). The existence of tortuous pockets, with cul-de-sac, which eventually become isolated, may favor the formation of abscesses .

The marginal closure of a periodontal pocket, may lead to an extension of the infection into the surrounding periodontal tissues due to the pressure of the suppuration inside the closed pocket. The fibrin secretions leading to the local accumulation of pus may favor the closure of the gingival margin to the tooth surface. Changes in the composition of the microflora, bacterial virulence, or in host defenses (Kareha et al. 1981) could also make the pocket lumen inefficient to drain the increased suppuration.

The development of a periodontal abscess in periodontitis may occur at different stages during the course of the infection: As an acute exacerbation of an untreated periodontitis (Dello Russo 1985)During periodontal therapy (Dello Russo 1985, Carranza 1990)In refractory periodontitis (Fine 1994) or During periodontal maintenance (Chace & Low 1993, McLeod et al. 1997)

Different mechanisms behind formation areExacerbation of chronic lesions: Occur without any obvious external influences.

B. Post therapy periodontal abscess Post scaling periodontal abscess occur immediately after scaling or routine prophylaxis. due to inadequate scaling which will allow calculus to remain in the deepest pocket area,

while the resolution of the inflammation at the coronal pocket area will occlude the normal drainage and then cause the abscess formation. When the periodontal abscess occurs immediately after scaling or after a routine prophylaxis, it has been related to the dislodging of calculus fragments, which can be pushed into the tissues.

Post-surgery periodontal abscess. Incomplete removal of sub gingival calculus or the presence of foreign substance. Ex-sutures, regenerative devices or periodontal pack. clinical study on guided tissue regeneration reported that 10 out of 80 controls (non-resorbable barrier) and 4 out of 82 tests (bio-absorbable barrier) showed abscess formation or suppuration at the treated sites.

(Garrett et al 1997)

Post-antibiotic periodontal abscess. Treatment with systemic antibiotics without subgingival debridement in patients with advanced periodontitis may also cause abscess formation.

It is Attributed to a likely change in the composition of subgingival microbiota, leading to a super infection and massive inflammation.

Topell et al (1990) reported on the development of multiple abscess (4-10) in 10 untreated periodontal patients who received systemic antibiotic therapy. (Penicillin, tetracycline) for non-oral infections.

Helovuo et al. (1993) studied 72 patients with untreated periodontitis, who were followed for 12 weeks, after intake of systemic antibiotics for non-oral reasons. Patients were divided into 3 groups according to the antibiotic used,

10 out of 24 patients (42%) in the penicillin group developed abscesses within the next 4 weeks. The number of abscesses ranged between 1-10. No abscesses were detected in the erythromycin or the control groups. Koller-Benz et al. (1992) showed that after initiation of nifedipine therapy, 8 abscesses appeared in 5 days. The nifedipine therapy was discontinued, and the abscesses resolved. 3 weeks later the treatment was resumed, and after 2 weeks another abscess was detected.

2. Periodontal abscesses in the absence of PeriodontitisImpaction of foreign bodies. Periodontal abscesses caused by foreign bodies, related with oral hygiene aids, have been named "oral hygiene abscesses. Perforation of the tooth wall by an endodontic instrument (Carranza 1990) Infection of lateral cysts (Kareha et al. 1981)Local factors affecting the morphology of the root may predispose to periodontal abscess formation

PATHOGENESIS AND HISTOPATHOLOGYThe entry of bacteria into the soft tissue pocket wall could be the first event to initiate the periodontal abscess.Inflammatory cells are then attracted by chemotactic factors released by the bacteria, and The concomitant inflammatory reaction leads to destruction of the connective tissues, the encapsulation of the bacterial infection and the production of pus.

Histologically, the intact Neutrophils are found surrounding a central area of soft tissue debris and destroyed leukocytes. At a later stage a pyogenic membrane, composed of macrophages and neutrophils is organized. The rate of destruction in the abscess will depend on the growth of bacteria and its virulence as well as the local pH, since an acidic environment will favour the activity of lysosomal enzymes

De Witt et al. (1985) studied biopsy punches taken from 12 abscesses. They observed, from the outside to the inside: (a) A normal oral epithelium and lamina propria; (b) An acute inflammatory infiltrate; (c) An intense foci of inflammation (neutrophil-lymphocyte) with the surrounding connective tissue destroyed and necrotic; (d) A destroyed and ulcerated pocket epithelium; (e) A central region, as a mass of granular, acidophilic, and amorphous debris.

MICROBIOLOGY The most frequent type of bacteria were gram-negative anaerobic rods and gram-positive facultative cocci. In general, gram-negatives predominated over gram-positives and rods over cocci. The periodontal abscess microbiota is usually indistinguishable from the microflora found in the subgingival plaque in adult periodontitis.The microflora from abscesses and deep pockets was similar and harbored higher proportions of pathogens when compared to the microflora of shallow pockets.

Bacterial species with capacity of producing proteinases, such as P. intermedia, are important, since they may in- crease the availability of nutrients, and thereby, increasing the number of bacteria inside the abscess (Jansen & Van der Hoeven 1997)

Culture studies of periodontal abscesses have revealed high prevalences of Porphyromonas gingivalis (55-100%), Prevotella intermedia (25-100%), and Fusobacterium nucleatum (44-65%) other pathogens Which have been reported are Actinobacillus actinomycetemcomitans (25%)Campylobacter Rectus (80%) Prevotella Melaninogenica (22%)

Clinical Features

Smooth, shiny swelling of the gingiva Painful, tender to palpationPurulent exudateIncreased probing depthMobile and/or percussion sensitiveTooth usually vital

DIAGNOSISDiagnosis should be based on Patients chief complaintClinical signs and symptoms Additional information can be obtained through a careful medical and dental history, and radiographic examination. Symptoms range from light discomfort to severe pain, tenderness of the gingiva, swelling, tooth mobility, tooth elevation, sensitivity of the tooth to palpation

Another common finding is suppuration, either spontaneous or after pressure on the abscess combined with rapid tissue destruction and deep pocket formation. The radiographic examination may reveal a normal appearance, or some degree of bone loss, ranging from a widening of the periodontal space to a dramatic radiographic bone loss. Systemic involvement has been reported in some severe cases, including fever, malaise, leukocytosis and regional lymphadenopathy.

Van Winkelhoff et al (1985) established 4 diagnostic criteria Association of pocket of >/= 6 mm, Presence of bleeding on probing, Evidence of radiographic bone loss & Absence of periapical lesion.

Other recommended additional diagnostic tools: include the use of Dark-Field Microscopical examination of the abscess microflora in order to exclude an endodontic origin, due to the higher percentage of spirochetes in periodontal abscesses. Positron Emission Tomography and a Fluorine-18-Fluoromisonidazole marker for detection of periodontal abscesses and other anaerobic infections in the mouth. Results from the clinical study showed that 100% of periodontal abscesses were found with this procedure.

DIFFERENTIAL DIAGNOSIS

Gingival abscessPeriapical abscess, Lateral periodontal cyst, Pericoronitis Vertical root fracture, Osteomyelitis Eosinophilic granuloma

Periodontal abscessGingival abscess Involves supporting periodontal structure Confined to marginal and / or interdental gingiva. Often occurs in the course of chronic destructive periodontitis Occurs in previously disease free areas. X-ray- bone loss present Acute inflammatory response to forcing of foreign material into the gingiva. No bone lossPocket present No pockets

Periodontal abscessGingival abscessPain diffuse.Pain dull May affect the entire side of the face.localized.Affected by thermal changes Not affected by thermal changes.

Periodontal abscessPeriapical abscessAssociated with preexisting periodontal pockets, caries or both. Associated with deep restoration, caries or Tooth wearPulp test- vital. Non-vital Swelling generalized and located around the involved tooth and gingival margin, seldom with a fistulous tract. Swelling localized often with fistulous tract opening in the apical area.

Periodontal abscessPeriapical abscessPain dull, constant, less severe, localized and patient usually can locate the offending tooth Pain - severe, throbbing, last for long, deep, unable to locate the offending tooth Pain associated with the movement or percussion is not as severe as with a pulpal disease Severe than periodontal abscess. Lateral radiolucencyApical radiolucency

Periodontal abscessPeriapical abscessAngular bone defects, Furcation involvementEndodontic filling or Endodontic or post perforationsResponds dramatically well to sub gingival debridement.Responds poorly or not at all to periodontal therapeutic interventions

Periodontal cyst (non-infected) No inflammatory signs More common in mandibular canine premolar region On radiograph well defined oval radiolucency on the lateral surface of the root, with chronic border, < 1 cm in diameter. Microscopically thin, non-keratinized stratified squamous epithelia with focal epithelial thickening. Inflammatory cells seen if secondarily infected.Treatment Enucleation.

Pericoronitis Usually seen in incompletely erupted tooth Commonly associated with mandibular 3rd molar. Osteomyelitis Rapid diffuse bone destruction may occur with in a few days Deeper pain being only symptom.X-ray indistinct trabecular and disappearance of lamina dura As infections increases, lymphadenopathy, fever and malaise are more common.

Eosinophilic granulomaDiagnosed by the rapid bone destruction after periodontal therapy Biopsy. Vertical root fractureLoupes or operating microscopes assist in visualization of cracks/fractures The bite test, Transillumination with fiber optic light and use of dyes helps in detecting the suspected fracture

Differential diagnosis should also be made with self-inflicted gingival injuries. Some lesions caused by patient's habits can mimic periodontal abscesses, such as trauma of the gingiva with a pencil (Rodd 1995) or with a safety pin (Beckett et al. 1995)A careful evaluation is the main factor to solve these cases, since conventional treatments usually fail unless the habit is discontinued.

TREATMENTTreatment of acute periodontal abscess usually involves two stages Management of the acute lesion. The appropriate treatment of the original and / or residual lesion, once the acute situations has been controlled.The purpose of treatment of acute periodontal abscess isAlleviate pain, Control the spread of infection, and To establish drainage.

Protocol recommended.Incision and drainage (closed or open approach) Scaling and Root planning Compression and debridement of soft tissue wall.Use of different systemically administered antibioticsTooth extraction.

Incision and drainage Through the pocket (Closed approach) Incision from the outer surface (Open approach)

Closed approach Anesthesia Flat instrument /probe carefully introduced into the pocket. Distend the pocket wall for drainage. Further drain and gently curettage the mass of tissue internally.

Open approach Vertical incision through the most fluctuant part of the swelling, extending to an area just apical to the abscess. Curette the granulomatous tissue internally. External aspect of the abscess is gently pushed to drain the remaining pus. Saline irrigation Approximate to wound margin No sutures required.

Antibiotic administrationMetronidazole 200 mg, tid, 5 days Smith and Davies(1986)Tetracycline 1 gm / day 2weeks -Hafstrom(1994)Azithromycin, 500mg, OD, 3 days.Amoxicillin + Clavulanate, 500 + 125 mg, tid, 8days.

Chronic periodontal Abscess Surgical therapy Gingivectomy Flap procedures Mainly in abscess associated with deep vertical defects, where the resolution of the abscess may only be achieved by a surgical operation. Objective : To eliminate the remaining calculus and to obtain drainage at the same time.

For the treatment of Gingival Abscess, the protocol should include the following: Elimination of the foreign object, through careful debridement (Abrams 1983)Drainage through the sulcus with a probe or light scaling, Rinsing with warm saline and follow-up after 24-48 hours

COMPLICATIONS Tooth LossSuggested as the main cause for extraction in the maintenance phase. History of repeated abscess formation is considered as a hopeless prognosis for the tooth. In a retrospective study, 45% of teeth with periodontal abscesses in a maintenance population were extracted (McLeod et al. 1997)

Dissemination of the infectionTwo possibilities have been described: I. The dissemination of the bacteria during therapy (bacteraemia); or II. Bacteraemia related with an untreated abscess.

The Dissemination of the bacteria during therapySuzuki & Delisle (1984) related a case of pulmonary actinomycosis due to a periodontal abscesses, which was ultra-sonically scaled. it was suggested that during treatment, Actinomyces sp. from the subgingival microflora had passed to the lungs.

Gallaguer et al. (1981) described a healthy patient with a periodontal abscess who was treated with drainage and curettage, but without systemic antibiotic. 2 weeks later a brain abscess was diagnosed, Microbiology of the lesions demonstrated, among other bacteria, Bacteroides melaninogenicus and other bacteroides, species.

II.Bacteraemia related with an untreated abscess.Cellulitis in breast cancer patients has been claimed to follow gingivitis or an abscess (Manian 1997) due to transient bacteraemia and reduced host defenses (radiation therapy and axillary dissection). The breast and the upper extremities are particularly susceptible to infections of oral origin (Manian 1997)periodontal abscess is also associated with the development of a cervical necrotizing fascitis. it is frequently associated with oropharyngeal infections.

Necrotising cavernositis:- Inflammation and necrosis of the Corpora Cavernosa or Corpus Spongiosum of male external genital organ leading to impotency. Culture from corposa carvernosa showed Peptostreptococcus species and Fusobacterium species. ( Pearle and Wendel 1993)

Sickle cell crisis in patient with sickle cell anemia: A periodontal abscess may also cause a sickle cell crisis, in patients with sickle cell anaemia (Rada et al. 1987)During the crisis, the abscess must be treated with antibiotics, aiming to avoid pain and to prevent dissemination of the infection. Definitive treatment should be delayed until resolution of the crisis.

Gingival Abscess

A localized purulent infection that involves the marginal gingiva or interdental papilla

Gingival Abscess

EtiologyAcute inflammatory response to foreign substances forced into the gingivaClinical FeaturesLocalized swelling of marginal gingiva or papillaA red, smooth, shiny surfaceMay be painful and appear pointedPurulent exudate may be presentNo previous periodontal disease

TreatmentElimination of foreign object

Drainage through sulcus with probe or light scaling

Follow-up after 24-48 hours

Pericoronal Abscess

A localized purulent infection within the tissue surrounding the crown of a partially erupted tooth.Most common adjacent to mandibular third molars in young adults; usually caused by impaction of debris under the soft tissue flap

Pericoronal Abscess

Clinical Features

Operculum (soft tissue flap)Localized red, swollen tissueArea painful to touchTissue trauma from opposing tooth commonPurulent exudate, trismus, lymphadenopathy, fever, and malaise may be present

Treatment Options

Debride/irrigate under pericoronal flapTissue recontouring (removing tissue flap)Extraction of involved and/or opposing toothAntimicrobials (local and/or systemic as needed)Culture and sensitivityFollow-up

The treatment of pericoronal abscess is aimed at

Managemant of acute abcess,followed by

Resolution of the chronic condition.

The acute pericoronal abscess is properly anaesthetizedDrinage is established lifting the soft tissue operculum with periodontal probe or curretteIf the underlying debris is accessible, It must be removed-followed gentle irrigation

Systemic antibiotics are given- swelling,regional lymphadenopathy.The patient is then instructed to rinse with warm water for every 2 hours and reassesed for 24 hours.Analgesics also prescribed-discomfort.

Acute phase has been controlled, the partially erupted teeth may be definitely treated with ;

Surgical excision of the overlying gingivaRemoval of the offending tooth.

CONCLUSION

REFERENCESClinical Periodontology : Carranza, Newman 9th EditionClinical Periodontology and implant dentistry Lindhe 4th edition Periodontal abscess: a review. JCDR-2011Periodontal Abscess review, JCP-2000, 27:377-386. Perio 2000 volume 34, 2004.