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Periodontal abscess  12
 

Periodontal abscess 12

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    Periodontal abscess  12 Periodontal abscess 12 Document Transcript

    • CONTENTS1. Introduction2. Definitions3. Classification4. Prevalence5. Etiology6. Clinical features7. Pathogenesis8. Histopathology9. Microbiology10. Diagnosis/differential diagnosis of periodontal abscess11. Investigations12. Treatment13. Complications14. Conclusion 1
    • Periodontal AbscessPeriodontal abscess is a frequent condition causing rapid loss of connective tissue.It is a condition where patient may seek immediate treatment.Definition: - Defined as lesion with an expressed periodontal breakdown, occuring during alimited 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.Classification: -1) Depending on location (Gillette & Banhous 1980, Carranza 1990)Periodontal abscessesGingival abscesses2) Depending on course – (Galego – Feal et al 1995 & Carranza 1990)Acute abscessesChronic abscesses3) Depending on number (Topoll et al 1990)SingleMultiplePrevalence: - Among all emergency dental conditions, periodontal abscesses represent approx8% of all dental emergences in Spain & 14 in USA (Ahl et al 1986). In UK periodontalabscess was diagnosed in 6-7% of all parts treatment in 1 month (Lewis et al) & was thirdmost prevalent emergency after dentoalveolar abscess (14-25%) & periocoronitis (10-2
    • 110%). Periodontal abscess is more prevalent in periodontitis patients. A periodontalabscess is more likely to occur in presenting pockets (Carranza). Teeth with abscesses areusually considered to have hopeless prognosis (Becker et al 1994).Etiology: - − 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. a. Acute exacerbation of untreated periodontitis (Dello Ruso 1985). b. During periodontal treatment (Dello Ruso & Carranza) c. Refractory periodontitis (Fine 1994) d. 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)3
    • May also be due to inadequate scaling which will allow calculus to remain indeepest pocket area, with resolution of inflammation at coronal pocket area whichoccludes normal drainage & causes abscesses formation (Dello Ruso 1985, Carranza1990). • 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 a. 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) b. Perforation of tooth by endodontic instrument. (Carranza 1990, Abrams et al 1992) c. Infected lateral cysts (Kareha et al 1981).4
    • d. Local factors affecting morphology of root may predispose to periodontal abscess formation. Presence to cervical cemental tears has been related to rapid progression ofperiodontitis & abscesses development (Haney et al 1992, Ishikawa et al) presence ofexternal root resorption (Yusof & Ghazali 1989), an invaginated tooth (Chen et al) or acracked tooth (Goose 1981) have been suggested as predisposing factors.3. Furcation involvement: - Abscesses are frequently found in furcation (Cohen).In majority of cases ofabscesses furcation involvement is found (Smith et al 1986). In a study by Yang 1987most periodontal abscesses occur in molar about 92.5%. Periodontal abscesses areprimary reason for molar extraction. Furthermore when loss of abscessed teeth wascompared between furcated & non furcated teeth, more furcated teeth were lost than nofurcated teeth. (Carranza)4. Diabetes: - Predisposition of pats with diabetes to purulent infection makes them prone toacute periodontal abscesses. Systemic alteration includes lowered host response, impairedimmunity, decreased leukocyte chemotaxis & bactericidal activity. Diabetes also havevascular changes & altered collagen metabolism which may increase susceptibility toabscess formation. Enhanced interaction of advanced glysation end products with theircellular receptor (RAGE) is suggested as one of pathogenic mechanism of acceleratedperiodontal disease in diabetes (Lalla, Hamster et al 1998)Pathogenesis & Histopathology − 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).5
    • Histopathology: -Intact neutrophils are found surrounding a central area of soft tissue debris & destroyedleukocytes.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 oflysosomal enzyme (De Witt et al 1985).De Witt et al 1985 studied biopsy punches from 12 abscesses & found from outside toinside. a. A normal oral epithelium & lamina propria. b. An acute inflammatory infiltrate c. An intense focus of inflammation (Neutro-Lymhpo) with surrounding CT destroyed & necrotic. d. A ulcerated & destroyed pocket epithelium e. A 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 CT Bacteria inside the abscesses were immersed in tissue exudates & surrounded bynecrotic tissue.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.6
    • • 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).Clinical factors:- − Two types clinically i.e. on course of lesion7
    • a) Acute:-− Appears avoid elevation of gingiva along lateral aspect of root.− Gingiva is edematous & rod 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 1986− McLeod et al showed 65% of affected teeth are multirooted− 10-40% 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.2. Chronic abscesses: -8
    • • Generally associated with sinus tract. Orifice of fistula may be covered by small granulation pink mass • Usually 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 abscesses − Lateral periapical cysts − Vertical root fracture − Endo perio abscesses − Post op infection − Osteomyelitis (Parrish et al 1989) − Gingival squamous cell carcinoma (Torabinejad & Rick 1980) − Metastatic carcinoma of pancreatic origin (Selelen et al)9
    • − Eosinophilic granulomaTreatment: - Acute abscess treatment includes 2 stages. (Ammons 1996) − Management of acute lesion − Appropriate 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) a. Drainage through pocket b. Scaling of tooth surface c. Compression & debridement of soft tissue wall & irrigation with saline. d. Pat should rinse with when saline & examined after 24-48 hrs. e. 1 week later definitive treatment should be given. Drainage could need external incision or flap & topical antiseptic application afterdrainage (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 beestablished. 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 & metronidazale − Hafstrom (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. 1. Importance of drainage 2. Potential for regeneration10
    • − 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.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 abscesses − Suzuki & 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)Gingival abscess: - − Localised, painful, rapidly expanding lesion involving marginal gingiva or interdental papilla sometimes in a previously disease free area. − Usually an acute inflammatory response to foreign substances forced into gingiva & in its early stages appears as red swelling with smooth, shining surface. − In 24-48 hrs the lesion is usually fluctuant & pointed, exudate may be expressed.11
    • − If permitted to progress the lesion gradually ruptures. − Symptoms include pulpal hypersensitivity.Treatment includes: − Elimination of foreign object through careful debridement (Abrams & Kopczyle 1983) − Drainage through sulcus with a probe or light scaling − Rinsing with warm saline & follow up after 24-48 hrs.Conclusion: - − Periodontal abscess is 3rd most frequent dental emergency, representing 7-14% of all dental emergencies & 6-7% of all pats seen in clinics − Higher prevalence has been found with 59% of untreated pats 13.5% during active treatment 37% during maintenance phase − 2 main etiologies should be distinguished 1. Those related to preexisting periodontal pockets 2. Those which do not necessarily need a deepened pocket. − Possible etiologies include 1. Exacerbation of existing disease 2. Post therapy abscesses 3. Re emergence of cured disease 4. Super infection 5. Impaction of foreign objects 6. Factors altering root morphology − Microflora related with periodontal abscesses is complex dominated by gr-ve strict anaerobic rods such as P. gingivalis, P. intermedia & F. nucleatum − The periodontal abscess has possibility to spread microbes to other body sites.12
    • − Tooth with periodontal abscess has worst prognosis & has higher chance of being lost − Three therapeutic approaches have been discussed 1. Drainage & debridement 2. Systemic antibiotics with or without other treatments 3. Periodontal surgeryReferences 1. Carranza’s clinical periodontology (10th edition) 2. Consensus report: Abscesses of the periodontium Ann. Periodontol pg. 83, Vol. 4. no. 1. Dec. 1999 3. Treatment of periodontal abscess in Adult Patients Presenting for Dental Care in The Oral Health Services Ministry Of Health Malaysia 2003 4. Clinical and microbiological characterization of periodontal Abscesses Jaramillo A, J Clin Periodontol 2005; 32: 1213–1218 5. The periodontal abscess: a review Herrera D, Rolda´n J Clin Periodontol 2000; 27: 377–386 6. Systemic anti-infective periodontal therapy- A systemic review-Haffajee,Ann periodontology-2003 7. The periodontal abscess (I). Clinical and microbiological findings Herrera D, Rolda´n J Clin Periodontol 2000; 27: 387–39413