periodontal abcess

Upload: periodontics07

Post on 16-Oct-2015

50 views

Category:

Documents


0 download

DESCRIPTION

periodontal abcess

TRANSCRIPT

  • *

  • CONTENTSINTRODUCTION DEFINITION AND PREVALENCECLASSIFICATIONETIOLOGY OF PERIODONTAL ABSCESSMICROBIOLOGYPATHOGENESIS AND HISTOPATHOLOGYCLINICAL FEATURES DIAGNOSISDIFFERENTIAL DIAGNOSISMANAGEMENT OF PERIODONTAL ABSCESSCONCLUSIONREFERENCES*

  • INTRODUCTION*

  • A Periodontal abscess (also termed lateral abscess, or parietal abscess), is a localized collection of pus (i.e. an abscess) within the tissues of the periodontium. It is a type of dental abscess. A periodontal abscess occurs alongside a tooth, and is different from the more common periapical abscess, which represents the spread of infection from a dead tooth (i.e. which has undergone pulpal necrosis). To reflect this, sometimes the term "lateral (periodontal) abscess" is used. In contrast to a periapical abscess, periodontal abscesses are usually associated with a vital (living) tooth. Abscesses of the periodontium are acute bacterial infections classified primarily by location.*

  • DEFINITION

    Defined as lesion with an expressed periodontal breakdown, occuring during a limited period of time & with easily detectable clinical symptoms (Hafstorm et al, 1994) with localized accumulation of pus located within gingival wall of periodontal pocket. (Carranza et al 1990)Synonym Lateral abscesses; parietal abscesses.*

  • PREVALENCE3rd most frequent dental emergencyRepresenting 7-14%Affecting 6-7%

    Effects prognosis of toothGray et al 1994- 27.5% and 59.5%Mc Leod et al 1997- 37%*

  • Among all emergency dental conditions, periodontal abscesses represent approx 8% of all dental emergences in Spain & 14 in USA (Ahl et al 1986). In UK periodontal abscess was diagnosed in 6-7% of all parts treatment in 1 month (Lewis et al) & was third most prevalent emergency after dentoalveolar abscess (14-25%) & periocoronitis (10-110%). Periodontal abscess is more prevalent in periodontitis patients. A periodontal abscess is more likely to occur in presenting pockets (Carranza). Teeth with abscesses are usually considered to have hopeless prognosis (Becker et al 1994).

    *

  • CLASSIFICATIONBased on durationBased on numberBased on location

    Based on etiologyPeriodontitis relatedNon- periodontitis related*

  • 1) Depending on location (Gillette & Banhous 1980, Carranza 1990)Periodontal abscessesGingival abscesses2) Depending on course (Galego Feal et al 1995 & Carranza 1990)Acute abscessesChronic abscesses 3) Depending on number (Topoll et al 1990)SingleMultiple

    *

  • PERIODONTITIS RELATED ABSCESSActive periodontal destructionExacerbation of a chronic lesionPost therapy periodontal abscessPost scalingPost surgeryPost antibiotic(Topoll in 1990)(Helevou et al in 1993-broad spectrum antibiotics)*

  • Four types of abscess associated with periodontal tissuesGingival abscessPeri-coronal abscessCombined periodontal/ endodonticLateral Periodontal abscess*{Periodontal abscess: A review Punit Vaibhav Patel, Sheela Kumar G, Amrita Patel}

  • NON PERIODONTITIS RELATED ABSCESSImpaction of foreign bodyOrthodontic devices

    Root morphology alterationsInvaginated root(Chen et al in 1990)Fissured root(Goose 1981)Root tears(Haney et al 1992)Endodontic perforations(Abrams et al 1992)*

  • ETIOLOGY OF PERIODONTAL ABSCESS*

  • Have been either directly associated to periodontitis or to sites without prior existence of periodontal pockets.A}Perio abscesses in periodontitis: -In periodontitis abscesses represent a period of active bone destruction.Existence of tortuous pockets with cul-de-sac which eventually becomes isolated may favour formation of abscesses (Carranza 1990)Marginal closure of pocket may lead to extension of infection into surrounding PDL tissue due to pressure of suppuration in closed pocket (Newman & Sims 1979)Fibrin secretion, leading to local accumulation of pus may favour closure of gingival margin to tooth surface (Galego-Feal et al 1995).

    *

  • Changes in composition of microflora, bacterial virulence or in host defence could also make pocket lumen inefficient to drain (Kareha et al 1981).Abscesses in periodontitis may occur at various stages.Acute exacerbation of untreated periodontitis (Dello Ruso 1985).During periodontal treatment (Dello Ruso & Carranza)Refractory periodontitis (Fine 1994)During periodontal maintenance (Chace & Low 1993, McLeod et al 1991).When periodontal abscess occurs immediately after scaling & or after routine prophylaxis it is related to dislodging calculus fragment deep into tissue. (Dello Russo 1985)

    *

  • May also be due to inadequate scaling which will allow calculus to remain in deepest pocket area, with resolution of inflammation at coronal pocket area which occludes normal drainage & causes abscesses formation (Dello Ruso 1985, Carranza 1990).Abscesses immediately after therapy have been reported clinical study of GTR membrane both resorbable & nonresorbable by Garett et al 1997 reported 10 out of 84 (NR barriers) & 4 out of 82 (R-barriers) showed abscesses or suppuration.Treatment with systemic antibiotics without subgingival debridement in pats with advanced periodontitis may cause abscess (Helovuo & Pacurio 1989 & Topoll et al 1990). This has been attributed to likely change in composition of subgingival microbiota leading to super infection (Helovuo et al 1993)Nifedipine therapy has also been attributed to abscess formation (Koller Benz et al 1992). A case report should that after initiating therapy 8 abscesses appeared in 5 days. Nifedipine was discontinued & drainage was done. The abscesses resolved 3 weeks later drugs were again started & after 2 weeks abscess was detected. NO clear cut explanation for cause & effect relationship is given.

    *

  • B. PERIODONTAL ABSCESSES IN ABSENCE OF PERIODONTITIS

    Impaction of foreign body (Kareha et al 1981), such as orthodontic elastics (Piniprato et al), piece of floss (Abrams & Kopczyk 1983), popcorn kernel (Rada et al) dislodged cemental tear (Haney et al 1992); corn husk in peri-implant tissue (Ibbott et al 1993); & unknown objects. Periodontal abscesses caused by foreign body, related with oral hygiene aids have been named oral hygiene abscesses (Gillette & Van House 1980)Perforation of tooth by endodontic instrument. (Carranza 1990, Abrams et al 1992)Infected lateral cysts (Kareha et al 1981).Local factors affecting morphology of root may predispose to periodontal abscess formation.Presence to cervical cemental tears has been related to rapid progression of periodontitis & abscesses development (Haney et al 1992, Ishikawa et al) presence of external root resorption (Yusof & Ghazali 1989), an invaginated tooth (Chen et al) or a cracked tooth (Goose 1981) have been suggested as predisposing factors.

    *

  • 3. Furcation involvement: -Abscesses are frequently found in furcation (Cohen).In majority of cases of abscesses furcation involvement is found (Smith et al 1986). In a study by Yang 1987 most periodontal abscesses occur in molar about 92.5%. Periodontal abscesses are primary reason for molar extraction. Furthermore when loss of abscessed teeth was compared between furcated & non furcated teeth, more furcated teeth were lost than no furcated teeth. (Carranza)

    *

  • 4. Diabetes: -Predisposition of pats with diabetes to purulent infection makes them prone to acute periodontal abscesses. Systemic alteration includes lowered host response, impaired immunity, decreased leukocyte chemotaxis & bactericidal activity. Diabetes also have vascular changes & altered collagen metabolism which may increase susceptibility to abscess formation. Enhanced interaction of advanced glysation end products with their cellular receptor (RAGE) is suggested as one of pathogenic mechanism of accelerated periodontal disease in diabetes (Lalla, Hamster et al 1998)

    *

  • ENVIRONMENTAL FACTORSPocketPre existing pocketMajor factorDeeper, narrower, tortuous*

  • MICROBIOLOGYAnaerobes (Newman& Sims)P. gingivalis- 50-100%(Topoll et al in 1990)*Periodontal pathogens usually isolated from periodontal abscessF nucleatumB forsythusP gingivalisP intermedia

  • Herrera et al in 2000- 45% anaerobes resembles periodontitis microbiotaPolymicrobial, non motile, gram negative, rod shaped anaerobesAshimoto et al- P gingivalisOther microbes includeP intermediaP melaninogenicaF nucleatumB forsythusSpirochetes*

  • Microbiology: Periodontal abscesses microflora is composed mainly of periodontal pathogens, especially P. gingivalis, P. intermedia, F. nucleatum, P. micros & B. forsythus.Newman & Sims 1979 studied a abscesses & found 63.1% of flora was strict anaerobes. Topoll et al reported 59.5% & David Harerra reported 45.1% of anaerobic flora.Percentage of Gram ve was 59.6% & rods was 72.2% in Newman & Sims study where as David Harrera (2000) reported 44.7% Gram -ve & 44.7% rod in their study.Total count of bacteria was approx to 1.35x106 bacteria in a study by Hafstrom et al.Black pigmented bacteria were found as most prevalent group of bacteria P. gingivalis 55-100% (Topell et al; Ashimoto et al, Newman & Sims et al 1979). P. intermedia 25-100% (Topell et al 1990, Newman & Sims 1979); P. melanogenica 0-22% Newman & Sims 1979 Van Winkelhoff et al 1985 and Hererra found 50%, 62.5% & 16.7% respectively.

    *

  • F. nucleatum has shown high prevalence 44.6-65% (Topell et al 1990, Haffstorm et al 1994) & 70.8% (Harrerra et al 2000).B. forsythus in 47.1% of pats (Harrerra et al) & 14.3% of patients (Ashimoto et al 1998) P. micros were found in 70.6% of pats (Harrerra et al 2000). No other study has reported so. P. micros is found in patients with periodontitis (Rams et al 1992)C. rectus was found in 4.2% of patients (Harrerra et al) & 80% (Hafstorm et al 1994) patients.P. gingivalis represented the highest percentage when present 13.6% of total flora (Harrerra et al 2000) percentages ranging 10.4% to 22% have been reported (Topell et al 1990, Newman & Sims 1979).Lower properties of P. intermedia are reported 8.5% (Harrerra et al 2000) & 4.4-7% by (Haffstorm et al 1994).S. viridans is most common isolate when aerobic Tech is used (Epstein 1977).Spirochetes have been found as predominant cell type (mean 40.6% 10.9%) when dark field microscopy was sued (Trope et al 1988).Strains of Peptostreptococcus, S.milleri, Bacteroide. capillosus, Vellionela, B. fragalis & E. corrodens have been isolated (Chen 1983)Disappearances of P. gingivalis from abscessed sites after treatment suggest close association of these microbes with abscess (Hafstrom 1994).

    *

  • OTHER LOCAL FACTORSForeign material such asPop-corn huskImpacted foodFish boneTooth brush bristlesIrrigating devices

    ANACHORETIC EFFECT*

  • PATHOGENESIS*

  • Entry of bacteria into pocket wall could be the first event.Inflammatory cells are then attracted by chemotactic factors released by bacteria & the inflammatory reaction leads to tissue destruction (De Witt et al 1985).There is subsequent encapsulation of bacterial infection & production of pus (Carranza 1990).

    *

  • HISTOPATHOLOGYDe Witt et al in 1985*

  • Intact neutrophils are found surrounding a central area of soft tissue debris & destroyed leukocytes.Later stage a pyogenic membrane composed of macrophages & neutrophils is organized.The rate of destruction in abscesses will depend on growth of bacteria inside the foci & its virulence as well as local pH, since acidic environment will favour activity of lysosomal enzyme (De Witt et al 1985).De Witt et al 1985 studied biopsy punches from 12 abscesses & found from outside to inside.A normal oral epithelium & lamina propria.An acute inflammatory infiltrate An intense focus of inflammation (Neutro-Lymhpo) with surrounding CT destroyed & necrotic.A ulcerated & destroyed pocket epitheliumA central region as a mass of granular acidophilic & amorphous debris. In 1 out of 9 specimen evaluated by EM, gram negative bacteria were seen invading the pocket epithelium & altered CTBacteria inside the abscesses were immersed in tissue exudates & surrounded by necrotic tissue.

    *

  • CLINICAL FEATURES AND DIAGNOSISAcute AbscessLocalized red, ovoid swellingPeriodontal pocketMobilityTooth elevation in socketTenderness to percussion or bitingExudationElevated temperatureRegional lymphadenopathy (Smith and Davies 86)*

  • Appears avoid elevation of gingiva along lateral aspect of root.Gingiva is edematous & red with smooth shining surface.Pus may be expressed from gingival margin by gentle digital pressure.Symptoms may vary from slight discomfort to severe pain & swelling. (Smith & Davis 1986).Feeling of pressure in gums is common.There is increase mobility, elevation of tooth in socket & tenderness to percussion or mastication.Regional lymphadenopathy can be detected in some people.Bleeding on probing is present in 66% of cases.Pockets present are deeper than 6mm in (62.1%) cases while 4-6mm in (34.4%) cases (Harrerra 2000)Regarding mobility (Smith & Devis 1986) 56.5% to 79% (Harrerra et al 2000) of teeth showed mobility.

    *

  • Molars are most commonly involved teeth 69% of cases (Harrerra et al 2000)Similar involvement is reported by Gray et al 1994 & slightly lower by Smith & Davis 1986McLeod et al showed 65% of affected teeth are multirooted10-40% pats show regional lymphadenopathy (Harrerra et al 2000, Smith & Davis 1986)In a study by Harrerra (2000)periodontal abscesses were seen 41% associated with first molar, 24% with seemed molar; 17% upper premolars; 7% lower premolars; 7% incisors & 3.5% upper third molars.55% abscesses were found in upper jaw & 48% are located on buccal aspect 24% distal aspect, 13.8% on lingual / palatal & mesial aspect 62% complained severe pain.

    *

  • Chronic AbscessNo pain or dull painLocalized inflammatory lesion Slight tooth elevationIntermittent exudationFistulous tract often associated with a deep pocketUsually without systemic involvement

    *

  • Generally associated with sinus tract. Orifice of fistula may be covered by small granulation pink massUsually asymptomatic although patients can refer mild symptoms (Carranza 1990)An acute abscess becomes chronic when drainage is established naturally through sinus tract or sulcus.Patients may have dull or gnawing pain, slight elevation of tooth & desire to bite tightly of grind.

    *

  • DIAGNOSIS

    Should be made after overall evaluation & interpretation of patients chief complaint; medial / dental history, clinical & radiographic examination.Radiographs & pulp test may give additional information relative to etiology of swelling.Clinically avoid elevation of gingiva along lateral aspect of root (Carranza 1990)Symptoms range from light to sever discomfort, tenderness of gingiva, swelling tooth mobility, tooth elevation.Radiographically may reveal normal appearance / some degree of bone loss & increase width of PDL space.

    *

  • DIFFERENTIAL DIAGNOSIS(Ahl et al 1986, Barletta 1988)Periapical abscessesLateral periapical cystsVertical root fractureEndo perio abscessesPost op infectionOsteomyelitis (Parrish et al 1989)Gingival squamous cell carcinoma (Torabinejad & Rick 1980) Metastatic carcinoma of pancreatic origin (Selelen et al)Eosinophilic granuloma*

  • MANAGEMENT OF PERIODONTAL ABSCESS*The treatment of the periodontal abscess usually includes two stages: (1) The management of the acute lesion, and (2) The appropriate treatment of the original and/or residual lesion, once the emergency situation has been controlled

  • Acute abscess treatment includes 2 stages. (Ammons 1996)Management of acute lesionAppropriate management of original or residual lesion.If tooth severely damaged prognosis is bad & has to be extracted (Smith & Devis 1989 & Ammon 1996)Protocol includes (Ammon 1996 & Ahl et al 1986)Drainage through pocketScaling of tooth surfaceCompression & debridement of soft tissue wall & irrigation with saline.Pat should rinse with when saline & examined after 24-48 hrs.1 week later definitive treatment should be given.

    *

  • Drainage could need external incision or flap & topical antiseptic application after drainage (Carranza 1990).Addition of systemic antibiotics is not well defined. Systemic antibiotic are advised only when there is clear systemic involvement need for premedicationWhen infection is not well localize Cases in where adequate drainage cannot be established. Some authors recommend combination of basic treatment & antibiotics (Galeyo Feal et al)Combination of I/D + systemic antibiotics has been considered as successful (Genco 1991)Penicillins are drug of first choice followed by amoxycillin & metronidazaleHafstrom (1994) suggested conservative treatment top gain as much attachment as possible. Drainage was done through pocket with saline irrigation & tetracycline was prescribed for 2 weeks (1 g/day). Two conclusions were suggested.Importance of drainagePotential for regeneration

    *

  • Chronic abscesses can be treated by surgical therapy i.e. gingivectomy & flap procedures. (Carranza 1990). Mainly abscesses associated with vertical bone defects where resolution of abscesses may only be achieved by surgical operation (Kareha et al 1981).Surgical flaps are proposed in cases of post prophylaxis abscesses to gain good debridement.

    *

  • *Draining the abscess with digital pressureIncision and drainage (Ahl et al 1986)Scaling and root planingTHE MANAGEMENT OF THE ACUTE LESION

  • ANTIBIOTICS*Antibiotic Options for Periodontal Infections1Antibiotic of ChoiceAmoxicillin, 500 mg1.0-g loading dose, then 500 mg tid, 3 days

    Penicillin AllergyClindamycin 600-mg loading dose, then 300 mg qid, 3 daysAzithromycin (or clarithromycin)1.0-g loading dose, then 500 mg qid, 3 days

  • Smith and Davies in 1986- metranidazole (200mg tid 5days)Herrera et al in 1994- tetracycline therapyThere was a rapid control of pain levels, reduction in edema, redness and swelling, periodontal probing depth were significantly reduced.

    GingivectomySurgical flaps*

  • COMPLICATION:

    1. Tooth loss: -Seen in cases of advanced to moderate periodontitis (Chace & low 1993, McLeod et al 1997).Tooth with H/O repeated abscesses is considered with other findings, a tooth with hopeless prognosis (Becker et al 1984)2. Dissemination of infectiona. Bacteremia following treatment of abscessesSuzuki & Delisle 1984 related a case of pulmonary actinomycosis due to periodontal abscess.Brain abscess was reported by Gallauger et al in case of periodontal abscess treated by drainage & curettage.The risk of bacteremia during drainage of an abscess can be reduced if, before incision a needle aspiration of content of abscess is done (Roberts & Sheriff 1990, Flood et al 1990)

    *

  • CASE REPORT BY KRITHIKA ET AL IN 2011CLENCHING ABSCESS*

  • RECENT STUDIESIf untreated the periodontal abscess may lead to cervicofacial necrotizing fasciitisMedeiros et al 2012Orthodontic Elastic Separator-Induced periodontal Abscess: A Case Report*Talia Becker and Alex Neronov in 2012

  • CONCLUSION*

  • Periodontal abscess is 3rd most frequent dental emergency, representing 7-14% of all dental emergencies & 6-7% of all pats seen in clinicsHigher prevalence has been found with59% of untreated pats13.5% during active treatment 37% during maintenance phase2 main etiologies should be distinguished Those related to preexisting periodontal pockets Those which do not necessarily need a deepened pocket.Possible etiologies includeExacerbation of existing disease Post therapy abscessesRe emergence of cured disease Super infectionImpaction of foreign objectsFactors altering root morphology

    *

  • Microflora related with periodontal abscesses is complex dominated by gr-ve strict anaerobic rods such as P. gingivalis, P. intermedia & F. nucleatumThe periodontal abscess has possibility to spread microbes to other body sites.Tooth with periodontal abscess has worst prognosis & has higher chance of being lost Three therapeutic approaches have been discussed Drainage & debridement Systemic antibiotics with or without other treatmentsPeriodontal surgery

    *

  • REFERENCESNewman, Takei, Klokkevld, Carranza,; Carranzas clinical periodontology. 10th Ed. 714Jan Lindhe, Niklaus P Lang, T Karring; Clinical periodontology and implant dentistry 5th edPeriodontal Abscess- A Review - (2000) Herrera. D, Journal of Clinical Periodontology: 27; 377-387.Periodontal Abscess etiology and classification-(1999)-Meng H. - Annals of Periodontology;79-82 Predominant Cultivable Microbiota- Newman et al.(1979).Journal of Periodontology;27;350-354Ashimoto. PCR detection of Periodontal/ endodontal pathogens associated with abscess formation (1998) - Journal of Dental Research 77; 854-858.*

  • Topoll HH, Lange DE and Miller RF: Multiple periodontal abscesses after systemic antibiotic therapy. J Clin Periodontol 1990; 17: 268-272.Krithiga Gurumoorthy, Babitha Ajjappa, Shobha Prakash; multiple acute periodontal abscesses due to clenching.: Journal of Interdisciplinary Dentistry / Jan-Jun 2011 / Vol-1 / Issue-1Saygun I, Yapar M, ozdemir A, Kubar A, Slots J. Human cytomegalo virus and Ebstien Barr virus type 1 in periodontal abscesses: oral microbiol Immunol 2004: 19: 83-87Cervicofacial necrotizing fasciitis following periodontal abscess. Medeiros Junior, Rui De Sousa Catunda, IvsonVieira Queiroz, Isaac Henrique Araujo de Morais, Hecio Carneiro Leao, Jair Alcino Monteiro Gueiros, Luiz: general dentistry jul/aug 2012. Vol 60 issue 4, 316-321Norhidayah, Khamiza What Expert Says Periodontal Abscess Malaysian Dental Journal (2008) 29(2) 154-157Obradovi R. Radmila, Kojovi B. Draginja, Brankovi R. Vesna: The Therapy Of Periodontal Abscess: Acta Stomatologica Naissi, Jun/June 2008, Vol. 24, Broj/Number 57.Talia Becker and Alex Neronov: Orthodontic Elastic Separator-Induced Periodontal Abscess: A Case Report; case reports in dentistry 2012*

  • **