Acute Gingival Infections.pptx

Acute Gingival Infections
features and treatment of each with articles

1. Management of Acute Gingival Infections Dr. Rinisha Sinha MDS Part II Department of Periodontology

2. Introduction Necrotizing ulcerative gingivitis (NUG) Primary herpetic gingivostomatitis Pericoronitis Articles Conclusion References Contents

3. Introduction INFECTION - The lodgment and multiplication of a parasite in or on the tissue of a host constitute infection. It does not invariably results in disease. An acute lesion is of sudden onset and short duration and is painful . They are manifested with severe pain along with systemic manifestations . The inflammatory response initiated in gingival disease appears to be prerequisite for destruction of connective tissue attachment apical to CEJ. Thus these lesions must be treated at the earliest with a proper treatment protocol. Acute lesions in the periodontium, such as abscesses and necrotizing periodontal diseases , are among the few clinical situations in periodontics where patients may seek urgent care, mostly due to the associated pain. Reference: Page et al. 1997

4. Acute Gingival Infections NECROTISING ULCERATIVE GINGIVITIS PRIMARY HERPECTIC GINGIVOSTOMATITIS PERICORONITIS ABSCESSES IN THE PERIODONTIUM Reference: Perry R. Klokkevold; Fermin A. Carranza Reference: David Herrera, Bettina Alonso, Lorenzo De Arriba, Isabel Santa Cruz, Cristina Serrano & Marino Sanz; Periodontology 2000; 2014

5. A microbial disease of the gingiva that most often occurs in an impaired host . Necrotizing ulcerative gingivitis , necrotizing periodontitis, necrotizing stomatitis are the most severe inflammatory periodontal disorders caused by plaque bacteria . They are rapidly destructive and debilitating and represents various stages of same disease process. Characterized by death & sloughing of gingival tissue & presents with characteristics signs & symptoms. NECROTISING ULCERATIVE GINGIVITIS Reference: Horing & Cohen 1995

6. Historical Perspective 1 st Event 2 nd Event 3rd Event 4 th Event 5 th Event 6 th Event In 4th BC In 1778 In 1886 In 1890s In 19 th Century 1999 American Academy of Periodontics classification system Recognized by Xenophon who stated that Greek soldiers were plagued with sore, ulcerated and foul-smelling mouths John Hunter first delineated the clinical differences between NUG, scurvy, and chronic periodontitis Hersch described that increased salivation, enlarged lymph nodes, fever and malaise had been associated with NUG Plaut and Vincent described the disease and attributed its origin to fusiform bacilli and spirochetes NUG occurred as an EPIDEMIC Acute Necrotizing Ulcerative Gingivitis (ANUG), now classified under Necrotizing Periodontal Disease

7. Synonyms Ulceromembranous gingivitis Acute necrotizing ulcerative gingivitis Trench mouth Vincent’s gingivostomatitis Phagedenic gingivitis Fusospirallary periodontitis Plaut -Vincent stomatitis Reference: Pickard 1973, Johnson & Engle 1986, Horing & Cohen 1995

8. ACCORDING TO PINDBORG Stage 1: Erosion of only tip of interdental papilla Stage 2: Lesion extending to marginal gingiva and causing potentially a complete loss of papilla Stage 3: Involving attached gingiva Stage 4: Exposure of bone Grading and Staging ACCORDING TO HORNING AND COHEN Stage 1 : Necrosis of tip of the interdental papilla (93%) Stage 2 : Necrosis of entire papilla (19%) Stage 3 : Necrosis extending to gingival margin (21%) Stage 4 : Necrosis extending to attached gingiva (1%) Stage 5 : Necrosis extending to buccal / labial mucosa (6%) Stage 6 : Necrosis exposing alveolar bone (1%) Stage 7 : Necrosis perforating skin and check (0%)

9. Clinical Features Punched out appearance of papillae Gray Pseudomembranous Slough Severe pain; sensitive to touch Spontaneous bleeding Initially lesions at the tip of the papillae and cols Generally seen first in the mandibular anterior region and third molar flaps. Narrow erythematous zone seen in between the marginal necrosis and unaffected gingiva- linear erythema Pronounced foetor ex ore and metallic taste Recession, rather than pocket formation Direct contact may cause lip and tongue ulcers Pharyngeal involvement- Vincent’s angina Seasonal variations Reference: Pickard 1973, Johnson & Engle 1986, Horing & Cohen 1995

10. Typical punched-out papilla between the mandibular canine and lateral incisor is covered by a grayish white pseudomembrane . More advanced case shows the destruction of the papillae, which results in an irregular marginal contour. Typical lesions with spontaneous hemorrhage. Generalized involvement of the papillae and the marginal gingiva with whitish necrotic lesions

11. Extraoral and Systemic Signs and Symptoms Local lymphadenopathy High Fever Increased pulse rate, leukocytosis, loss of apetite and general lassitude additionally seen in severe cases Insomnia, constipation, GI disorders, headache and mental depression in children Other Severe Sequalae Severe sequalae of Gangrenous Stomatitis Fusospirochetal meningitis Peritonitis Pulmonary infection Toxemia Fatal brain abscess Noma Reference: Berke JD 1961, Box HK 1930, Enwonwu CO 1972, Jimenez M 1975

12. Zone 1 Bacterial zone Zone 2 Neutrophil rich zone Zone 3 Necrotic Zone Zone 4 Zone of Spirochetal Infiltration Histopathology Reference: Listgarten 1993

13. ROLE OF BACTERIA Prevotella Intermedia , Fusobacteria , Treponema, Selenomonas The specific cause of NUG has not been established. The prevalent opinion is that it is produced by a complex of bacterial organisms but requires underlying tissue changes to facilitate the pathogenic activity of bacteria. Plaut and Vincent in 1894 and 1896 , respectively introduced the concept NUG is caused by specific bacteria – namely a fusiform bacillus and a spirochetal organism . Rosebury and coworkers described a fusospirochetal complex consisting of T. marcodentium , intermediate spirochetes, vibrios , fusiform bacilli and filamentous organisms in addition to several Borrelia species More recently Loesche and colleagues described a constant flora and a variable flora. Etiology Reference: Cahn LR: The penetration of the tissue by Vincent’s organisms: a report of a case, J Dent Res 9:695–698, 1929. Courtois GJ, 3rd, Cobb CM, Killoy WJ: Acute necrotizing ulcerative gingivitis: a transmission electron microscope study, J Periodontol 54:671–679, 1983. Ellerman V: Vincent’s organisms in tissue, Z Hyg Infekt Pr 56:453,1907.

14. ROLE OF HOST RESPONSE Presence of organisms insufficient to cause disease NUG is not produced experimentally in humans and animals by inoculation of bacterial exudates from the lesion Characteristic lesions occurs in animals when they are under immunosuppression Not found in well nourished individuals with fully functional immune system Immunosuppression essential - NUG patients displayed depression in leukocyte chemotaxis and phagocytosis Nutritional deficiency, fatigue caused by chronic sleep deprivation, alcohol/drug abuse, psychological factors, systemic disease It is hence concluded that - The specific cause of NUG has not been established & it is produced by a complex of bacterial organisms but requires underlying tissue changes to facilitate the pathogenic activity of the bacteria. HIV Reference: Cogen et al, 1983

15. Local and Systemic Predisposing Factors Reference: Pindborg et al, 1951 Reference: Smith DT, 1932 Reference: Chapman OD, 1941; King JD 1942; Miller DK 1935 Reference: Gidmon DB, 1964 Reference: Goldhaber P, 1964 Reference: Shannon IL, 1969

16. Diagnosis Reference: By Genco, Goldman and Cohen

17. Herpetic Gingivostomatitis Chronic Periodontitis Desquamative Gingivitis Streptococcal Gingivitis Apthous Stomatitis Diptheric And Syphilitic Lesions Tuberculous Gingival Lesion Candidiasis Agranulocytosis Dermatoses (Pemphigus, Erythema Multiforme In Lichen Planus) Differential Diagnosis LITTNER MM IN 1982 STUDIED THAT BACTERIAL SMEAR SHOWS A PREPONDERANCE OF STREPTOCOCCAL FORMS, WHICH WERE IDENTIFIED AS STREPTOCOCCUS VIRIDANS, AND HE REPORTED IT TO BE GROUP A BETA HEMOLYTIC STREPTOCOCCUS.

18. Management

19. The treatment needs to be approached in successive stages: Treatment of the acute phase, Treatment of any preexisting condition, Treatment of disease sequelae, and Transition to supportive or maintenance phase. Treatment of the acute phase aims to halt tissue destruction and to control the patient's discomfort. gentle, ultrasonic debridement of superficial gingival plaques and calculi along with localized oxygen therapy, directed at necrotic lesions Reference: Malek R, Gharibi A, Khlil N, Kissa J. Necrotizing Ulcerative Gingivitis. Contemp Clin Dent. 2017 Jul-Sep;8(3):496-500 DUCKWORTH R (1966), LOESCHE WJ (1982) IN THEIR STUDY SHOWED THAT THE TREATMENT WITH METRONIDAZOLE RESULTS IN SIGNIFICANT REDUCTION OF TREPONEMA SPECIES, P.INTERMEDIA, AND FUSOBACTERIUM WITH RESOLUTIONS OF CLINICAL SYMPTOMS.

20. First Visit Complete evaluation and comprehensive medical history with special attention to recent illness, living conditions, dietary backgrounds, type of employment, hours of rest, cigarette smoking, stress levels, HIV Examination should include general appearance, presence of halitosis, skin lesions, vital signs, lymph node The involved area are isolated and then cleaned. The pseudomembrane and debris are removed with a moist cotton pellet where the lesion is isolated with a cotton swab and local anesthetic may be used. Ultrasonic scaling is done to remove the supragingival calculus. Subgingival scaling curettage are contraindicated because of possibility of bacteremia and extending the infection to deeper tissues. Patient is advised to rinse mouth twice daily with equal mixture of warm water to 3% hydrogen peroxide and twice daily rinse with 12% chlorhexidine for 30 days; adequate rest; confine toothbrushing to ultrasoft toothbrush and bland dentifrice. Antibiotics : Amoxicillin 500 mg every 6 hrs. or (Erythromycin 500 mg every 6 hrs.) along with Metronidazole 250 mg three times daily for 7 days. Patient is also advised to avoid tobacoo , alcohol and condiments. Patient is recalled after 1-2 days. Reference: Martos J, Ahn Pinto KV, Feijó Miguelis TM, Cavalcanti MC, César Neto JB. Clinical treatment of necrotizing ulcerative gingivitis: a case report with 10-year follow-up. Gen Dent. 2019 May-Jun;67(3):62-65 Oral penicillin was demonstrated in one study to show significant clinical improvement in three to six days. Reference: Malek R, Gharibi A, Khlil N, Kissa J. Necrotizing Ulcerative Gingivitis. Contemp Clin Dent. 2017 Jul-Sep;8(3):496-500; Walker C, 2002

21. Second Visit Patient condition – usually improved. Pain is diminished or no longer present. Areas still erythematous but without pseudomembrane Shrinkage of gingiva – expose calculus which is then gently removed. Instruction same as previous visit. Reference: Martos J, Ahn Pinto KV, Feijó Miguelis TM, Cavalcanti MC, César Neto JB. Clinical treatment of necrotizing ulcerative gingivitis: a case report with 10-year follow-up. Gen Dent. 2019 May-Jun;67(3):62-65

22. Third Visit 5 days after 2 nd visit Patient should be symptom free Repeat scaling and root planing Discontinue hydrogen peroxide mouthwash but continue CHX mouthwash Patient instructed in plaque control procedures Counselling on nutrition, habits Reference: Dufty J, Gkranias N, Donos N. Necrotising Ulcerative Gingivitis: A Literature Review. Oral Health Prev Dent. 2017;15(4):321-327 Reference: Wennstrom J, 1969

23. Subsequent Visits Tooth surfaces in the involved areas are scaled and smoothened. Plaque control is checked and corrected if required. Patient should now be scheduled for treatment of chronic disease. Appointments are scheduled for the treatment of the gingivitis, periodontal pockets, and peri coronal flaps as well as for elimination of all forms of local irritation. The third molar flaps and other nidi of infection are eliminated. Gingivoplasty and osseous surgery is done if the lost gingival architecture is not regained after nonsurgical therapy. Reference: Malek R, Gharibi A, Khlil N, Kissa J. Necrotizing Ulcerative Gingivitis. Contemp Clin Dent. 2017 Jul-Sep;8(3):496-500

24. AIM: To report a case of orthodontic patient with refractory ANUG successfully treated with topical probiotic L. Reuteri . CASE PRESENTATION: A 16-year-old female reported to a private practice. Anamnesis was positive for celiac disease , and the patient observes a gluten-free diet , but does not eat fruit and vegetables . She was in orthodontic treatment and she developed a particular gingivitis and reported strong gingival pain, spontaneous gingival bleeding and persistent halitosis . The onset of gingivitis occurred after a few months from the beginning of orthodontic treatment . No radiographic lesions were appreciable. A clinical diagnosis of necrotic ulceration gingivitis was performed . The patient was submitted to local antiseptics, without improvement , so the dentist has prescribed antibiotic therapy but the patient has never performed this therapy .

25. CASE PRESENTATION: They therefore had tried to treat this condition with periodontal debridement every 3 months, for several months but had not a total remission and episodes of exacerbation were present . It confirmed even more the diagnostic hypothesis that it is not a classical gingivitis. They had decided to associate a treatment with topical probiotics Lactobacillus reuteri DSM 17938 and lactobacillus reuteri ATCC PTA 5289 to the non-surgical periodontal therapy . The treatment was performed in 4 appointment . In the first session, recording of periodontal clinical parameters, debridement and topical application of probiotics in suspension were made . Systemic probiotics of Lactobacillus Reuteri taken at home 2 times a day was prescribed. The probiotic used was a 5 ml suspension in drops The solution was injected into the pockets until the spill , for 3-5 minutes and at the end the patient did not rinse the mouth and was advised not to eat and drink for about an hour. CASE PRESENTATION: The probiotic tablet has to be dissolved slowly in the mouth after oral hygiene for four weeks of treatment . In the second session , topical application of suspended probiotics and hygiene motivation was performed. At this appointment the patient presented plaque , but despite this, improvement was visible with reduction of the bleeding . In the third and fourth session , the patient was submitted to another topical application in suspension of probiotics . At 6 weeks the patient healed and orthodontic appliance was removed . At 4 months a follow up visit was performed. The clinical parameters before and after probiotic therapy confirm the result.

26. CONCLUSION The use of topical probiotics in the treatment of gingivitis and ANUG could be considered a valid alternative to conventional treatments for refractory cases in patients in orthodontic therapy, for their effectiveness and safety . Further studies, especially randomized clinical trials, must be performed to confirm this starting result.

27. The objective of this study was to quantitatively compare the bacterial population structure in plaque from the gingival margin of two groups of 21 Chinese patients with gingivitis or necrotizing ulcerative gingivitis (NUG). Subjects were recruited in four dental clinics in Eastern China. Samples were quantitatively assessed by immunofluorescence and fluorescent in situ hybridization for taxa known to be associated with periodontal diseases. The analyses showed that the fusiform taxa (Fusobacterium nucleatum /Fusobacterium periodonticum , Leptotrichia buccalis , Tannerella forsythensis , and Capnocytophaga sp.), Campylobacter rectus, Prevotella intermedia, Prevotella nigrescens , Selenomonas sputigena , and treponemes were present in both groups with high prevalence. Porphyromonas gingivalis and Actinomyces gerencseriae were much more prevalent in the NUG group. Quantitatively, most taxa, including P. gingivalis , F. nucleatum and the treponemes , accounted, on average, for < 3% of the total bacterial cell number. Only P. intermedia/P. nigrescens , P. gingivalis , S. sputigena , A. gerencseriae , and the sum of all monitored suspected periodontal pathogens were significantly increased in the NUG group. The present study demonstrates for both groups a highly diverse plaque composition and suggests that, etiologically, the overall concentration and the concerted effects of the entire group of opportunistic pathogens thriving in NUG-associated plaque are of prime importance.

28. Caused by herpes simplex virus type 1(HSV 1). Occurs commonly in children and infants younger than 6 years of age , but is also seen in adolescents and adults. Virus ascends through the sensory and autonomic nerves where it persists as latent HSV. Primary infection is asymptomatic . Secondary manifestations results from various stimuli such as sunlight, trauma, fever, stress . These manifestations include herpes labialis, herpes stomatitis, herpes genitalis , herpetic encephalitis . PRIMARY HERPETIC GINGIVOSTOMATITIS Reference: A.H. Ajar, P.J. Chauvin, “Acute herpetic gingivostomatitis in adults: a review of 13 cases, including diagnosis and management,” J. Can. Dent. Assoc., vol.68, pp. 247-251, April 2002. Reference: Dodd K, 1938; Mcnair ST 1950 Reference: Cowson RA 1976, Scott TFM 1941

29. Clinical Features Oral signs : Diffuse, erythematous shiny involvement of gingiva and adjacent oral mucosa. Varying degree of edema and gingival bleeding. In initial stage  discrete spherical gray vesicles are seen on gingiva, labial and buccal mucosa, soft palate, pharynx, tongue and sublingual mucosa. After about 24 hrs , vesicles rupture forming painful ulcers with red, elevated, halo like margin and a depressed, yellowish or grayish white central portion. Course of disease limited to 7 to 10 days. Scarring does not occur in areas of healed ulcerations. Symptoms: Generalized soreness Inability to eat and drink Sites are sensitive to touch, thermal changes, foods such as condiments and fruit juices and action of coarse foods. Extra oral & systemic signs and symptoms: Cervical adentis Fever  101 F to 105 F (38.3ºC to 40.6ºC) Generalized malaise Reference: A.H. Ajar, P.J. Chauvin, “Acute herpetic gingivostomatitis in adults: a review of 13 cases, including diagnosis and management,” J. Can. Dent. Assoc., vol.68, pp. 247-251, April 2002. Reference: Kolokotronis A, Doumas S. Herpes simplex virus infection, with particular reference to the progression and complications of primary herpetic gingivostomatitis. Clin Microbiol Infect 2006;12:202–11.

30. Recurrent acute infection Episode may occur after febrile disease as pneumonia, meningitis, influenza, typhoid. It also tends to occurring during periods of anxiety, stress or exhaustion as well as during menstruation. Also occurs during early stage of infections mononucleosis. History

31. The virus targets the epithelial cells which show ‘ballooning degeneration’ consisting of acantholysis nuclear clearing and nuclear enlargement. These cells are called Tzank cells Infected cells fuse forming multinucleated cells and intercellular edema that leads to formation of an intra epithelial vesicles that rupture and develop a secondary inflammatory response with a fibropurulent exudate. Histopathology Reference: Amir J, Harel L, Smetana Z, Versona I; 1997

32. Diagnosis Reference: P. Jaya, K. Harijanti , “Gingivostomatitis herpetika primer ( laporankasus ),” Oral Med. Dent. J., vol. 1, pp. 6-9, June - December 2009

33. Difference ANUG PHGS 1. Bacterial etiology Viral etiology 2. Necrotizing condition Diffuse erythema and vesicles 3. Punched-out papillae and pseudomembrane Rupture of vesicles- spherical ulcers 4. Papillae and marginal gingiva Gingiva, buccal mucosa, lips 5. Uncommon in children Common in children 6. No definite duration 7 to 10 days 7. No immunity Immunity seen 8. Contagion not observed Contagion

34. Management Reference: Amir et al. Reference: Amir J, Harel L, Smetana Z, Versona I; 1997 Reference: Seigel MA, 2002 Reference: Abramowicz M, 2007

35. CASE PRESENTATION: A 36 year female patient reported with the main complaint of burning feelings in the mouth and wound formation in upper arch region since 7 days . Patient was apparently alright 7 days back, after which she developed a wound in the upper arch followed by fever for 2-3 days and the wound gradually increased in the size associated with pain and discomfort . Medical history revealed that she is suffering from hyperthyroidism since 5 years and is under medication. No relevant past dental history was found. She is of mixed diet and brushes once daily with toothbrush . General examination was done followed by systemic examination, extra-oral examination, TMJ examination, lymph node examination and intra-oral examination and no complications were found. Local examination revealed that an ulcer present on the mid of the head palate size 1x1cm and yellowish white in colour surrounded with erythmatous halo with irregular borders .

36. CASE PRESENTATION: Border was coalescing with adjacent ulcer of size 0.5x0.5 cm with no secondary changes evidence. Also presence of linear gingival erythema irt 46 47 and 48 region . On palpation all the inspector findings of size, site and shape were confirmed. The ulcer was smooth in consistency with flat border and was tender on palpation. Provisional Diagnosis In view of history record and medical discoveries a temporary diagnosis of Acute Herpetic Gingivostomatitis was specified. Differential Diagnosis Herpetiform apthous stomatitis Hypersensitive stomatitis Erythema multiforme Inflammations because of cancer therapy Primary ulcerative gingivitis Investigations Generally the analysis of AHGS is determined by the clinical information . CBC and ESR examinations were done and complications were not found .

37. CASE MANAGEMENT The patient was prescribed orally, Zovirax 200 mg 1 tablet four times daily for 5 days after food . Also advised to take Cap VCOR Gold 1cap for 10 days after food. After 5 days patient again prescribed to take Wysolone 10 mg 1 capsule thrice every day for 3 days followed by 1 capsule twice every day for 2 days and also instructed to apply Kenacort ointment thrice daily for 15 days . Patient was advised to take delicate and nutritious food and revisit afterward 15 days . On revisit, complete healing of lesion was seen. CONCLUSION Acute herpetic gingivostomatitis mainly seen in children but can also found in all age groups . This type of HSV infection is exceptionally transmissible . The distinctive signs of this condition are several ulcers and reddish gingival boundaries . Diagnosis broadly depend on the clinical discoveries and indications. Acute herpetic gingivostomatitis is inoffensive and self-limiting in immunocompetent situations . This infection is generally noticeable in the oral or buccal cavity region, that’s why it is significant for the dentist to diagnosis the disease in right time and deliver a suitable treatment to the patients.

38. Objectives:  To examine the efficacy of acyclovir suspension for treating herpetic gingivostomatitis in young children. Design:  Randomized double blind placebo controlled study. Setting:  Day care unit of a tertiary pediatric hospital. Subjects:  72 children aged 1-6 years with clinical manifestations of gingivostomatitis lasting less than 72 hours; 61 children with cultures positive for herpes simplex virus finished the study. Main outcome measures:  Duration of oral lesions, fever, eating and drinking difficulties, and viral shedding. Intervention:  Acyclovir suspension 15 mg/kg five times a day for seven days, or placebo. Results:  Children receiving acyclovir had oral lesions for a shorter period than children receiving placebo and earlier disappearance of the following signs and symptoms: fever , extraoral lesions (lesions around the mouth but outside the oral cavity); eating difficulties, and drinking difficulties. Viral shedding was significantly shorter in the group treated with acyclovir. Conclusions:  Oral acyclovir treatment for herpetic gingivostomatitis, started within the first three days of onset, shortens the duration of all clinical manifestations and the infectivity of affected children. Further studies are needed to evaluate the ideal dose and length of treatment.

39. Pericoronitis refers to inflammation of the gingiva in relation to the crown of an incompletely erupted tooth. Occurs most commonly in mandibular third molar area. TYPES : Acute Subacute Chronic PERICORONITIS

40. Clinical Features Space between crown and overlying gingival flap shows accumulation of food debris and bacteria; causing inflammation. Inflammatory fluid and cellular exudate increase the bulk of the flap, which then may interfere with complete closure of jaws or can be traumatized by contact with opposing jaw, aggregate the inflammatory involvement. Clinically it is seen as a markedly red, swollen, suppurating lesion that is exquisitely tender, with radiating pain to the ear, throat and floor of the mouth. Swelling of cheek in the region of angle of jaw and lymphadenitis are seen. Patient may also have toxic systemic symptoms such as fever, leukocytosis and malaise.

41. Management Reference: Amir et al. Extraction involves a risk of bone loss on distal surface of second molar. Operculectomy includes removal of distal wedge of the tissue along with the occlusal flap.

42. Complications

43. Aim : The aim of the study was to compare the effectiveness of operculectomy over removal of third molar for the management of pericoronitis. Materials and Methods: 150 healthy adults aged between 19 and 35 years , who reported to dental OPD for management of pain in third molar region and were further diagnosed with pericoronitis . All patients included in the study fulfilled the eligibility criteria for surgery under local anesthesia as per the American Society of Anaesthesiology (ASA) Class I . The protocol of this study was reviewed and approved by the Institutional Review Board. Written informed consent for the study was obtained from all patients. All procedures were carried out by the same surgeon .

44. Randomization Patients were randomly assigned to one of the two groups. Group-I :- Patients diagnosed with pericoronitis in relation to mandibular third molar and were subjected to conventional operculectomy technique . Group-II :- Patients diagnosed with pericoronitis in relation to mandibular third molar and were subjected for removal of third molar. 57 patients among them were men and 18 were women in group I . In group II 60 were men and 15 were women respectively. Assessment All the patients were evaluated by the same independent observer postoperatively on the 5th post-operative day to check the parameters of the study by comparing patient compliance on pain and wound healing between the two study groups.

45. Evaluation of wound healing The surgical sites were examined for delayed healing and signs of any infection. RESULT (ON THE 5 TH DAY POST-OPERATIVELY) Pain Out of 150 participants, 3 patients reported with pain in group I with a mean difference of 3.01 and a standard deviation of 1.33 and 32 patients in group II with a mean difference of 4.35 and a standard deviation of 1.54. Wound healing Out of 150 participants, 1 patient of group I had delayed wound healing with a mean difference of 2.97 and a standard deviation of 1.13 and 8 patients in group II had delayed wound healing with a mean difference of 3.12 and a standard deviation of 1.28. DISCUSSION & CONCLUSION Treatment of choice for management of pericoronitis remains controversial and challenging. Operculectomy (group I) as choice of treatment had favorable and positive outcome as there was faster wound healing and minimal discomfort experienced by our patients , however surgical removal (group II) can be considered as a treatment option as it eliminates the cause associated with pain in mandibular third molar but, the complication rates were found to be high and the method of operation seems iatrogenic. Operculectomy is a promising alternate technique for the management of pericoronitis in terms of patient compliance with minimal or no complications when compared to removal of third molar for the same reason.

46. Conclusion

47. References