Acute gingival infections

Department of Periodontics
Seminar
#Pericoronitis
#Acute necrotizing Ulcerative gingivitis (#ANUG)
#Herpetic Gingivo Stomatitis
3rd Year BDS
#Dentistry

1. Acute Gingival Infections Department of Periodontics By Aswanth.E.P

2. Contents Introduction Necrotizng Ulcerative Gingivitis Primary Herpetic Gingivostomatitis Pericoronitis Conclusion Reference

3. INTRODUCTION Necrotizing ulcrative gingivitis,pericoronitis and primary herpetic gingivostomatitis are some important acute gingival infections Necrotizing ulcerative gingivitis is a microbial disease of the gingiva in the context of an impaired host response Primary Herpetic gingivostomatitis is an infection of the oral cavity caused by herpes simplex virus (HSV) type 1 & 2 The term Pericoronitis rfers to inflammation of the gingiva in relation to the crown of an incompletely erupted tooth

4. Necrotizing Ulcerative Gingivitis( NUG ) It is an inflammatory disease of gingiva ,with charecteristic signs and symptoms. Also called Vincent’s infection,Trench mouth,Acute ulceromembraneous gingivitis… Identified as an acute disease. It can cause destruction of supporting structures. When it involve bone-bone loss-referred as Necrotizing ulcerative periodontitis ( NUP ).

5. Charecterized by acute onset , followed by an episode of debiliating diseases or acute respiratory tract infections. Acronym – ANUG Patient may have a history of smoking / malnutrition / recent history of stress like examination… / HIV + ve It can cause tissue destruction that involve peiodontal attachment apparatus,mainly in patients with long standing disease or severe immunosupression . When bone loss occurs,called necrotizing ulcerative periodontitis (NUP) Clinical features :

6. Oral Signs Lesions are punched out , crater like depressions at crest of interdental papillae ,subsequently involving marginal gingiva and rarely attached gingiva . These craters are covered by grayish pseodomembraneous slough,which is demarcated from the remaining of the mucosa by pronounced linear erythema . Ulcerations 2 type : 1)Lateral ulceration & necrosis 2)Deep ulceration & necrosis

7. Gingival hemorrhage or pronounced bleeding on slightest stimulation. Fetid odour & increased salivation NUG & NUP not lead to periodontal pocket formation as the necrotic changes involve junctional epithelium ; a viable junctional epithelium is needed for pocket deepening.

8. Oral symptoms : Lesions are extremely sensitive to touch . Complaints of constant radiating ,gnawing pain that is intensified by eating spicy or hot foods and chewing. Metallic foul taste present and patient conscious of an excess amount of pasty saliva. Extra oral signs & symptoms In mild-moderate stages,local lymphadenopathy & slight elevation in temperature. In severe cases,high fever,increased pulse rate,leukocytosis,loss of apetite & general lassitude are seen. Systemic reactions severe in children. Insomnia,GIT disorders,headache are associated.Rarely gangrenous stomatitis ,fatal brain abscess are reported

9. Clinical course : It can vary & if untreated ,NUG may lead to NUP,combined with severe toxic systemic complications. A disease is communicable if it can be passed on to another by natural modes of spread like direct contact,water … “Transmissible” denote capacity to maintain infectious agent in successive passagers through a suceptible host. As inoculation not produce ANUG ,it is transmissible but not communicable/ contigeous .

10. Etiology 1)Role of bacteria Plut & Vincent introduced the concept that NUG is caused by specific bacteria namely Fusiform bacillus & Spirochetal organisms. Rosebury et al described a fusospirochetal complex that consist of T.microdentium,intermediate spirochetes,vibrios ,..in addition to several Borrelia species. Loesche et al described predominant constant flora;consist of Prevotella intermedia in addition to Fuso bacterium,Treponema species & a variable flora consist of heterogenous array of bacterial types .

11. Bacteriological findings supported by immunological data,increased IgG and IgM titers to spirochetes & P.intermedia in patients as compared with healthy controls. 2)Role of host response : An impaired host response reported in NUG. Decreased resistance to infection,and physical and emotional stresses are earlier described with NUG. It has not been produced experimently by only inoculation of bacterial exudates from the lesions. Local or systemic immunosupression with glucocorticoids ( ketoconazole ) results in more charecteristic lesions in infected animals .

12. NUG not found in well nourished individuals with fully functional immune system. 3)Predisposing factors : All predeposing factors for NUG are associated with immunosupression . a)Local predisposing factors : Include : Pre-existing gingivitis Injury to the gingiva Smoking . Deep periodontal pockets & pericoronal flaps- favorable environment for anaerobic fusiform bacteria & spirochetes.

13. Areas of gingiva that are traumatized by opposite teeth( eg : palatal surface behind maxillary incisor..) are more prone to NUG. Smoking act as a factor because: Direct effect of tobacco in gingiva Vascular & other changes induced by nicotine( vaso constriction , endothelial injury) 3)Smoking and NUG are both reflctions of stress . Decreased chemotaxis & phagocytosis observed. b)Systemic predisposing factors : Nutritional deficiency Debiliating diseases Psychosomatic factors

14. 1)Nutritional deficiency : Poor diet is a predisposing factor as they depress leukocyte fuction . Vit.B & C deficiency accentuate the response of gingival tissues produced by increased bacterial flora. 2) Debiliating diseases : Chronic diseases – Syphilis,Cancer GIT disorders – Ulcerative colitis Blood dyscrasias – Leukemia,Anemia AIDS 3) Psychosomatic factors : Psychiatric distrubance lead to activation of hypothalamic-pituitary-adrenal axis .

15. This result in elevation of serum & urine cortisol levels. It associated with depression of lymphocytes & PMNL function that may predispose to NUG . Histopathology : Lesion involve both epithelium & connective tissue. Surface epithelium destroyed & replaced by pseudomembranous meshwork of fibrin,necrotic epithelial cells,PMNN … This zone clinically appeared as surface pseudomembrane . Immediate border of ths pseudomembrane,epithelium is edematous and individual cells exhibit varying degrees of hydropic degeneration. There is infiltration of PMNs in intercellular spaces.

16. Underlying connective tissue is markedly hyperemic with numerous engorged capillaries & dense infiltration of PMNs. Relation of bacteria to the NUG lesion : Zone 1-Bacterial zone : Most superficial Consist of varied bacteria including few spirochetes of small,medium & large type . Zone 2-Neutrophil rich zone : Contains numerous leukocytes , predomintly neutrophils Bacteria including spirochetes present between the leukocytes.

17. Zone 3 – Necrotic zone : Consist of disintegratedtissue cells,fibrillar materials, remnants of collagen fibers. Intermediate & large spirochetes with few other organisms present Zone 4 – Zone of spirochetal infiltration : Consist of well preserved tissue infiltrate with intermediate & large spirochetes without other organisms.

18. Diagnosis It is based on clinical findings of gingival pain, ulceration & bleeding. Bacterial smear not definitive as it is not appreciably different from that of patients with marginal gingivitis,periodontal pockets,pericoronitis or primary herpetic gingivostomatitis . Differential diagnosis include : 1) Gonococcal stomatitis 2) Agranulocytosis 3)Vincent’s angina 4) Desquamative gingivitis 5)NUG in leukemia & AIDS

19. Treatment At 1 st visit,topical anaesthetic applied & ulcer gently cleaned with cotton swab & pseudomembrane present on base of ulcer removed area by area. Supragingival scaling is adviced,preferably ultra .. Subgingival scaling not indicated as it cause discomfort to patient. If lymph adenopathy present ,Penicillin can be given.Also metronidazole . On next visit,pain usually subsidise & gingival margin devoid of pseudomembrane.Thorough scaling recommended. As gingival oedema reduced,more of calculus & deposits could be removed without much discomfort to the patient. Due to necrotizing ulcer,normal scalloping is diminished – favours food accumulation – recurrence of ANUG.Thus Gingivoplasty done. If pericoronal flaps present,removed by distal wedge surgery. Nutritional supplements – Vit.B /C supplements .

20. Acute Herpetic Gingivostomatitis (AHG) It is a viral infection caused by HSV-1 (mostly) & HSV -2 Occurs most often among infants & children who are <6years old,but is also seen in adults. No sex predilection. Primary infection is asymptomatic . In primary infection,virus ascends through sensory & autonomic nerves where it is persists as latent HSV in neuronal ganglia that innervate the site. Secondary results from stimuli like sunlight,trauma,fever & stress. Secondary manifestatons includes herpes labialis,herpetic stomatitis,herpes genitalis … It is a contigeous disease which may spread via direct contact…

21. Clinical features Oral signs It appears as diffuse,erythematous shony involvement of gingiva & adjacent oral mucosa with varying degrees of edema & gingival bleeding.

22. In initial stage,appears as discrete,spherical clusters of vesicles dispersed in different areas like labial & buccal mucosa,hard palate,pharynx … After 24 hours,vesicle reptures and form a shallow ulcer with scalloped borders & surrounding erythema . Diffuse,edematous enlargement of gingiva with tendency toward bleeding is seen. Course of disease limitted to 7-10 days.

23. Oral symptoms Generalized soreness of the oral cavity which interferes with eating & drinking. Ruptured vesicles are senstive to touch,thermal changes,fruit juices … Extraoral & Systemic signs & symptoms Cervical lymphadenopathy Fever Generalized malaise

24. Histopathology Central portion of acute inflammation charecterized by ulceration & varying degrees of purulent exudate,surrounded by zone rich in engorged blood vessels. Virus targets the epithelial cells which show “ balloning degeneration” that consist of acantholysis,nuclear clearing & nuclear enlargement. These cells called Tzanck cells. Infected cells fuse to form multinucleated cells & inter cellular edema leads to formation of intraepithelial vesicles that rupture & develop secondary immune response with a fibropurulent exudate .

25. Round eosinophillic inclusion bodies called “ Lipschutz bodies” are found in nuclei of epithelial cells . Connective tissue is infiltrated by plasma cells. Smear obtained is Tzanck smear & is stain using Giemsa’s stain. Diagnosis Established from patients’s history and clinical findings. HSV isolation by cell culture is the gold standard. PCR Tzanck smear

26. Differential diagnosis Erythema multiforme Necrotizing Ulcerative Gingivitis Recurrent aphthous ulcer Aphthous stomatitis . Treatment Primary gingivostomatitis is treated with lignocaine for pain relief. Acyclovir at 15mg/kg given 5 times a day for 5-7 days reduces duration of fever ,reduces infectivity and halts the progression of lesions.

27. Pericoronitis It refers inflammation of gingiva in relation to the crown of an incompletely erupted tooth. Mostly occurs in mandibular 3 rd molar area. 3 types : Acute Subacute Chronic Clinical features Space between the crown of tooth & overlying gingival flap is an ideal area for accumulation of food debris & bacterial growth.

28. Inflammatory involvement of pericoronal flap and adjacent structures are seen. Gingival tissue that extending to occlusal suface is called operculum. Inflammatory fluid & cellular exudate increase the bulk of flap which then interfere with complete closure of jaws & which in can be traumatized by contact with the opposing jaw,thereby aggrevating the inflammatory involvement. Red ,edematous ,suppurating lesion that is extremly tender with radiating pain to the ear,throat & floor of mouth. Patient uncomfortable as result of pain,foul taste,inability to close the jaws,…

29. Complications Involvement may become localized in the form of pericoronal abscess. If it occurs in partially erupted vital tooth,it may give rise to cyst formation. It may spread posteriorly into the oropharyngeal area & medially into the base of tongue,making it difficult for the patient to swallow. Swelling of cheek in the region of angle of jaw & lymphadinitis are common. Systemic complications include fever,leukocytosis & malaise.

30. Peritonsillar abscess formation,cellulitis & Ludwig’s angina are infrequent but nevertheless potential swquelae of acute pericoronitis . Treatment : At 1 st visit,area flushed with warm water to remove superficial debris & exudate followed by application of topical anesthetic agent . Flap is reflected with scaler & underlying debris is removed. If gingival flap is swallon & fluctuent,an antero -posterior incision to establish drainage .

31. In next visit,determination made as to whether the is to be retained or extracted. If it is decided to retain the tooth,surgical procedures Performed using peridontal knife / electrosurgery . Under anasthesia,wedge shaped incision made to section a tissue that include gingival flap with tissue distal to the involved tooth as well. After tissue removed,periodontal pack is placed.

32. CONCLUSION Acute gingival infections lead to severe discomfort and may lead to life –threatening complications , and therefore they need to be treated promptly Adequate patient education and motivation is necessary as patients do not complete the treatment once the acute phase has subsided .

33. Reference 1)CARANZA’S Clinical Periodontology : 2 nd edition By M G NEWAN,H H TAKEI , P R KLOKKEVDD , F A CARRANZE 2)Essentials of Clinical Periodontology & Periodontics by Shantipriya Reddy , 4 th edition.