Acute periodontal Infections

Part 1 of the seminar on Acute Periodontal Infections
By Dr. Ritam Kundu, MDS PGT, Dr. R. Ahmed Dental College & Hospital, Kolkata, India.

1. ACUTE PERIODONTAL INFECTIONS

2. Introduction Acute infections are of sudden onset , limited duration & with well defined features in contrast with chronic lesions. Associated with Pain . Early diagnosis & prompt treatment is necessary to prevent rapid destructions of periodontal tissues.

3. Acute Periodontal Infections Abscess in the Periodontium Pericoronitis Herpetic gingivostomatitis Bacterial acute infections ( e.g. Streptococcal gingivostomatitis , Gonococcal stomatitis ) NUG

4. An abscess is a cavity containing pus and surrounded by inflamed tissue, formed as a result of a localized infection. Periodontal abscess : 8-14% among all dental emergency condition - ( Ahl et al 1986, Galego-Feal et al, 1996) Abscess in the Periodontium

5. Classification proposed by Meng (1999), which was included in the revised classification system of periodontal diseases, developed by AAP- International Workshop for a Classification of Periodontal Diseases and Conditions (1999): Gingival abscess Periodontal abscess Pericoronal abscess

6. Gingival abscess : A localized, painful, rapidly expanding lesion involving the marginal gingiva or interdental papilla, sometimes in a previously disease-free area. Periodontal abscess : A localized accumulation of pus within the gingival wall of a periodontal pocket resulting in the destruction of the collagen fibre attachment and the loss of nearby alveolar bone. Pericoronal abscess : Localized accumulation of pus within the overlying gingival flap surrounding the crown of an incompletely erupted tooth.

7. Gingival Abscess: Etiology : Acute inflammatory response to foreign substances forced into the gingiva Impaction of foreign bodies (such as a piece of dental floss, a popcorn kernel, a piece of a toothpick, fishbone. Clinical Features: Localized swelling involving marginal gingiva or interdental papilla A red, smooth, shiny surface May be painful and appear pointed Purulent exudate may be present No previous periodontal disease

8. Treatment Treatment of gingival abscess is aimed at reversal of the acute phase and removal of the cause. 1. Topical or local anaesthesia by infiltration is administered. 2. When possible, SRP to establish drainage and remove microbial deposits. 3. In acute cases, the fluctuant area is incised with a #15 scalpel blade and exudate may be expressed by gentle digital pressure.

9. 4. Any foreign material is removed. 5. The area is irrigated with warm saline water and covered with moist gauze under light pressure. 6. Once bleeding has stopped, patient is dismissed with instructions to rinse with warm saline water every 2 hrs. 7. After 24 hrs, the area is reassessed, and if resolution is sufficient, scaling not previously completed is undertaken. 8. If the lesion is large or poorly accessible, surgical access may be required.

10. Periodontal Abscess

11. Periodontal Abscess - also known as a lateral abscess or parietal abscess. Definition: ‘A lesion with an expressed periodontal breakdown occurring during a limited period of time, and with easily detectable clinical symptoms, including a localized accumulation of pus located within the gingival wall of the periodontal pocket’ - Herrera D, J Clin Periodontol 2000 Etiology based Classification: Periodontitis related abscess: acute infections due to bacteria present at the subgingival biofilm in a deepened periodontal pocket Non-periodontitis related abscess: foreign body impaction, alteration in the root integrity leading to bacterial colonisation

12. Course of the lesion : Acute abscess : Pain, Tenderness, sensitivity to palpation and suppuration. Chronic abscess : normally associated with a sinus tract and it is usually asymptomatic or mild symptoms Acute Chronic Number of abscesses: Single periodontal abscess is usually associated with local factors, which contribute to the closure of the drainage of a periodontal pocket. Multiple periodontal abscesses have been reported in uncontrolled diabetes mellitus, in medically compromised patients and in patients with untreated periodontitis after systemic antibiotic therapy for non-oral reasons.

13. Clinical Features Smooth, shiny swelling of the gingiva Painful, tender to palpation Purulent exudate Increased probing depth Mobile and/or percussion sensitive Tooth usually vital

14. Pathogenic mechanisms related to abscess formation in the periodontium : A) Exacerbation of a chronic lesion : obstruction of a deepened pocket, mostly in spiral tortuous pocket. An untreated periodontitis patient Recurrent infection during SPT B) Post-scaling Periodontal Abscess: Dello Russo 1985: Shrinkage of gingival tissue post-scaling – small fragment of remaining calculus – obstructing the pocket entrance – abscess Small fragment of calculus – forced into deeper previously non- inflammed tissue C) Post-surgery periodontal abscess: Garrett et al 1997 Presence of fragments of suture or periodontal pack within the periodontal tissue following the surgical procedure D) Post- antibiotic periodontal abscess: Helovuo et al 1989, Topoll et al 1990 Systemic antibiotic with out appropriate subgingival debridement - subgingival biofilm protected from the action of the antibiotic – acute infection – abscess E) Non-periodontitis related abscess formation: Foreign body : oral hygiene devices ( bristle of tooth brush, tooth pick fragments) Orthodontic appliances Food particles, nails F) Anatomic Factors : Invaginated roots, presence of fissures, iartrogenic endodontic perforations

15. Microbiology of Periodontal abscess : Microbiota of periodontal abscesses is not different from the microbiota of chronic periodontitis lesions. It is polymicrobial and dominated by nonmotile , gram-negative, strictly anaerobic, rod-shaped species. Among these bacteria, P. gingivalis is probably the most virulent and relevant microorganism Other strict anaerobes - Prevotella intermedia, Prevotella melaninogenica , Fusobacterium nucleatum , Tannerella forsythia, Treponema spp. Parvimonas micra , Actinomyces spp. and Bifidobacterium spp. Facultative anaerobic gram-negative bacteria, Campylobacter spp., Capnocytophaga spp. and Aggregatibacter actinomycetemcomitans , as well as gram-negative enteric rods .

16. Diagnosis: Clinical feature Signs & Symptoms Clinical findings- deep periodontal pocket, BOP, Suppuration, Mobility ( occasional) Radiology: No R/F or just widened PDL spaces in acute cases Evident bone loss, furcation involvement in acute exacerbation of chronic cases Differential diagnosis: PA abscess, PA cyst, Endo – perio lesions Rare cases : Osteomyelitis in periodontitis patients, SCC, Metastatic tumor of head – neck region, Pyogenic granuloma

17. Treatment A) Management of acute condition: Establish drainage – localised abscess Via sulcus is the preferred method Surgical access for debridement - Incision and drainage Removal of foreign body Extraction : poor prognosis in SPT Local / Systemic Antibiotics – diffuse involvement B) Management of Residual lesion in CP patients

18. Antibiotic of choice: Herrera et al in 2000 - Amoxicillin + Clav . Acid ( 500 + 125 mg ) . TDPC * 8 Days And Azithromycin ( 500 mg * OD * 3 Days) Smith & Davies (1986) – Metronidazole ( 200 mg * TDPC * 5 Days) Hafstrom et al 1994 – Tetracycline therapy for 2 weeks Eguchi et al 2008 – Saline + 2% Minocycline hydrochloride ointment Antibiotics although showed reduction in pain, edema , suppuration. Incision, Drainage and Debridement is always the First line of treatment, unless there is diffuse involvement

19. Complications: Tooth loss : Chace & Low – 1993 : Abscess – main cause of extraction during SPT Dissemination of the infection : Suzuki & Delisle 1984 : Pulomonary actinomycosis Gallaguer et al 1981 : Brain abscess It has been suggested that the risk of bacteremia during abscess drainage may be reduced if a needle aspirate of the abscess contents is obtained before the procedure - Flood TR et al, 1990, Roberts GJ et al 1990

20. Pericoronitis It was first described by GUNNELL in1844 Corona means crown in latin . Pericoronitis - Inflammation of tissues surrounding the crown of the tooth Definition: An inflammatory condition of the gingiva in relation to the crown of an incompletely erupted tooth. (Carranza, 12 th Edition) It is an inflammation of gingiva & contiguous tissues about crown of an incompletely erupted tooth. ( Orban ) C/F: The partially erupted or impacted Mandibular third molar is the most common site. Maxillary Third molar, Mandibular First, Second Molars are also affected. The space between the crown of the tooth and operculum (i.e. overlying gingival flap) harbours food debris and promotes bacterial growth due its relative inaccessibility to the cleansing measures. The operculum, even in patients without any symptoms is chronically inflamed with ulcerations in the inner aspect Acute inflammation is a constant possibility, which is exacerbated by the factors like, trauma, occlusion from the opposing teeth or foreign body impaction

21. It is identified by varying degrees of inflammatory involvement of the pericoronal flap & adjacent structures as well as by systemic complications. The inflammatory fluid & cellular exudate increases the bulk of the flap, which may interferes with complete closure of the jaw & traumatized by contact with the opposing jaw. There is red, swollen, suppurating lesion that is tender, with severe throbbing intermittent pain, exaggerated by chewing & interfering with sleep. Pain radiates to ear, throat & floor of mouth. Foul taste, halitosis, & inability to close the mouth.

22. Subacute Stage Continuous dull ache, radiates infrequently Stiffness of jaws, intraoral swelling, unpleasant taste. Causes less systemic upset Trismus might be present

23. Complications: Involvement may be localised in form of pericoronal abcess Posteriorly spread to oropharynx Medially to the base of the tongue, thereby causing difficulty in swallowing Involvement of submaxillary , posterior & deep cervical, retropharyngeal lymphnodes Peritonsilar abcess , cellulits & Ludwig’s Angina are infrequent complications.

24. Treatment: Treatment depends on severity of the inflammation, systemic complications, Extraction or Non extraction Persistent asymptomatic pericoronal flap should also be removed as a preventive measure Gentle flushing with warm water to remove debris and exudate Swabbing with antiseptic after elevating the flap with a scaler Evaluation of the occlusion of the opposing tooth and adjustments if necessary. Antibiotics, in case of diffuse microbial infiltration. In case of fluctuant abscess drainage should be accomplished by incision. Post treatment monitoring is necessary to ensure the resolution of the acute phase. Extraction of the impacted tooth, if necessary.

25. Resection of some or all pericoronal tissue ( operculectomy ) depending on tooth position in the jaw & soft tissue relationships, reduces the chances of recurrent infection. Not only the Occlusal flap, the distal flap should also be removed, to make the area cleansable and free from pocket distally. Operculectomy – surgical removal of operculum. It can be done using hand instruments, or electrosurgery or LASER.

26. Herpetic Gingivostomatitis

27. HERPES SIMPLEX VIRUS Herpes simplex Virus is a DNA virus & is a member of the human herpes virus family (HHV) family known as herpetoviridae . TYPES Type 1 – HSV 1 – Oral manifestation Type 2 – HSV 2 – Ano -genital infections Other members of HHV family includes Varicella zoster virus ( HHV 3) Epstein barr virus ( HHV 4) Cytomegalo virus ( HHV 5) Others – HHV 6, HHV 7, HHV 8

28. HSV- type 1 Infants/ children younger than 6 yrs Male = Female Primary infection asymptomatic Virus – penetrates neural ending – retrograde transmission through the sensory or autonomic nerves – smmoth ER (200-300mm/day) – Trigeminal ganglia – Latent virus Sunlight, fever, trauma, stress , after oral surgical procedures

29. Secondary manifestations Herpes labialis Herpetic stomatitis Herpes genitalis Ocular herpes Herpetic encephalitis

30. Early stage After few days Late stage showing brownish crusted lesions Vermillion border and skin adjacent to it is affected, where the neural endings form cluster The lesion heals after about 2 weeks

31. Clinical features Diffuse, erythematous , shiny involvement of the gingiva and adjacent oral mucosa Varying degree of edema and gingival bleeding Discrete spherical grey vesicles Rupture of vesicles and formation of ulcers after 24 hrs Ulcers– small , painful, red, elevated, halo-like margin with depressed yellowish/ greyish white central portion Widely spread/clusters 7-10 days No scarring Primary herpetic gingivostomatitis

32. Soreness, difficulty in eating and drinking Ruptured vesicles sensitive to touch, thermal changes, foods such as condiments and fruit juices Infants show irritability and refusal to take food

33. Extra-oral Cervical adenitis Fever (101 ͦ -105 ͦ F) Generalized malaise

34. Histopathology Tzanck cells : Virus targeted epithelial cells - Ballooning degeneration ( acantholysis , nuclear clearing, nuclear enlargement) Lipschutz bodies : There is presence of intranuclear inclusion bodies. P eri inclusion halo : Nucleolar fragmentation occurs with the condensation of chromatin around the periphery of the nucleus. Intracellular edema - intraepithelial vesicles - vesicle ruptures Lesion demonstrate a surface fibrinopurulent membrane. There is secondary infiltration by inflammatory cells in subadjacent connective tissue.

35. Diagnosis Early diagnosis important History/clinical findings PCR : Rapid & Reliable Blood sample showing high antibody titer against HSV ( diagnostically evident only in case of primary infection, as the titer remains high through the the rest of the life) Virus culture Immunologic tests using monoclonal antibodies or DNA hybridization techniques

36. Differential Diagnosis Recurrent Aphthous stomatitis Small well defined round shallow ulcers, yellowish grey central areas & red halo H/o previous mucosal ulcers is diagnostic, unknown etiology Apthous does not affect keratinised mucosa, only lining mucosa is affected No diffuse erythematous involvement of the gingiva , no acute toxic symptoms

37. Communicability Contagious : Viral shedding Recent studies have demonstrated HSV in periodontal pockets (Slots J 2000) Herpetic Whitlows : Infection of fingers of health professional treating infected patients may occur

38. Treatment Consists of early diagnosis & immediate initiation of antiviral therapy. Diagnosis within 3 days of Primary HGS – Antiviral More than 3 days - (immunocompetent patient) - Limited value Antivirals : Acyclovir suspension 15mg/kg is given 5 times daily for 7 days (Amir et al,1997) Valacyclovir or Famiciclovir alternative DOC

39. Rationale of using Anti-viral Drug Immuno-deficeient patints with long term therapy with acyclovir – Resistance – Alternate DOC ( Westheim et al, 1987) Patient with recurrent herpes infection – prophylactic use of antiviral – prior to any dental treatment ( Miller et al, 2004 ) Acyclovir Placebo Fever 1 Day 3 Days New Extra oral lesions 5.5 Difficulty in eating 4 Days 7 Days Viral shedding 1 Day 5 Dyas * Amir et al 1997

40. Palliative measures: Removal of food debris, plaque and supra gingival calculus NSAID (FEVER AND PAIN) Extensive periodontal therapy to be postponed Local /systemic antibiotics to prevent opportunistic infection especially in immuno -compromised patients The patient must be informed that the disease is contagious , thus precautions must be taken (vesicles –highest viral titer) Supportive measures: Copious fluid intake Nutritional supplements Topical anesthetics while eating

41. Streptococcal gingivostomatitis Characterized by diffuse erythema of the gingiva and other areas of the oral mucosa Bacterial smears– streptococcal forms Streptococcus viridans , groupA ß -hemolytic streptococcus

42. Gonococcal Stomatitis Caused by Neisseria gonorrhoeae Mucosa is covered with a grayish membrane that sloughs off in areas to expose an underlying raw bleeding surface Most common in new born due to transmission through maternal passages

43. Agranulocytosis Characterized by marked decrease in number of circulating PMN’s No marked inflammation due to diminished defense mechanism Lesions similar to NUG Blood studies can be used to differentiate between NUG and agranulocytosis

44. Vincent’s angina Fusospirochetal infection of oropharynx and throat, which affects marginal gingiva . May extend to the larynx and the middle ear

45. Next Seminar …… NUG NUP NUP as a manifestation of systemic disease