Acute Necrotizing Ulcerative Gingivitis.pptx

Trench mouth, sometimes called acute necrotizing ulcerative gingivitis (ANUG), is a severe gum infection that spreads quickly. It is typified by the abrupt onset of significant bleeding, ulceration, and gum discomfort; these symptoms are frequently accompanied by a very bad breath odor. ANUG is frequently linked to immunosuppression, smoking, stress, and poor dental hygiene. Young individuals are usually affected by the illness, which if neglected can result in severe tissue loss. It is crucial to have prompt dental care, such as expert cleaning and antibiotic treatments, in order to control ANUG and stop subsequent issues.

1. ASSLAM O ALAIKUM…. TOPIC: Acute necrotizing ulcerative gingivitis

2. CONTENTS: INTRODUCTION ETIOLOGY CLINICAL FEALTURES HISTOPATHOLOGY ZONES OF ANUG STAGES OF ANUG DIAGNOSIS and D/D TREATMENT PLANS

3. ACUTE NECROTIZING ULCERATIVE GINGIVITIS: DEFINITION: Acute necrotizing ulcerative gingivitis is a microbial disease of gingiva in context to an impaired host response. Its an acute gingival infection (ANUG). Acute necrotizing ulcerative gingivitis is a painful infection of the gums. It is characterized by death and sloughing of gingival tissue.

4. INTRODUCTION: Severe necrosis of free gingival margins, gingival crest and the interdental papilla. Its also known as TRENCH MOUTH, because of its prevalence in soldiers working in trenches during WW1. Higher incidence occurs between 15 and 30 years. ANOTHER NAMES OF ANUG: (NUG) Vincent's disease Fusospirochetal gingivitis

5. Etiology : Borellia vincenti Fusiform bacilli PREDISPOSING FACTORS: LOCAL : Smoking (nicotine stimulates vasoconstriction of peripheral blood vessels and decrease phagocytic activity of leukocytes) Deep periodontal pockets SYSTEMIC FACTORS: Altered host response Systemic disease such as Anemia, Leukemia and AIDS. Nutritional deficiency states, poor nutritional habits and insufficient protein intake, vitamin C, B deficiencies Stress

6. CLINICAL FEATURES: The triad associated with ANUG is : Other symptoms are: Its an aggressive ulceration typically starting at the tip of the interdental papilla, spreading along the gingival margins, eventually destroying the periodontal tissue. 

7. Its chronic form dose not exist. Advanced form of ulcerative gingivitis causes destruction of bone, periodontal apparatus, especially patients who are immunocompromised. When periodontal loss occurs ANUG can transform into NUP or NOMA . Oral signs : Punched out lesions Crater like depressions at crest of interdental papilla Surface of crater covered by gray, pseudomembranous slough Erythema on gingiva Some lesions are denuded of surface pseudomembranous which exposes the gingival margins, which are shiny , red, and hemorrhagic.

8. SYSTEMIC SIGNS AND SYMPTOMS: Systemic lymphadenopathy Fever Increased pulse rate Leukocytosis Loss of appetite Insomnia Mental depression Headache GI disorders Constipation NOMA Systemic symtoms are more severe in childrens

9. VS

10. HISTOPATHOLOGY: Surface epithelium is destroyed and replaced by meshwork of fibrin, necrotic epithelial cells , polumorphonuclear leukocytes predominantly neutrophils and various types of microorganisms. Connective tissue is hyperemic with numerous engorged capillaries and dense infiltration of PMNs ,this acute inflamed zone appears clinically as the linear erythema beneath the surface pseudo membrane .

11. Zones of ANUG : Bacterial zone: It is the most superficial zone consists of varied bacteria including spirochetes. Neutrophil rich zone: Contains numerous leukocytes predominantly neutrophils and bacteria including spirochetes. Necrotic zone: Consists of dead tissue cells, remnants of connective tissue fragments and bacteria including spirochetes. Zone of spirochetes infiltration: Consist of a well preserved tissue infiltration with spirochetes without other organisms.

12. STAGES OF ANUG: Stages of oral necrotizing disease - by Horning & Cohen Stage 1- necrosis of the tip of the interdental papilla. Stage 2- necrosis of entire papilla Stage 3- necrosis extending to the gingival margin. Stage 4- necrosis extending to the attached gingiva. Stage 5- necrosis extending to labial & buccal mucosa. Stage 6- necrosis exposing alveolar bone. Stage 7- necrosis perforating skin of cheek.

13. DIAGNOSIS: Diagnosis based upon clinical features (DIAGNOSTIC TRIAD) ULCERATIONS PAIN FETID ODOUR AND BLEEDING

14. DIFFERENTIAL DIAGNOSIS: 1.Herpetic gingivostomatitis 2.chronic periodontitis 3.Desquamative gingivitis 4.Streptococal gingivostomatitis 5.Apthous stomatitis 6.Gonococal gingivostomatitis 7.diphtheritic and syphilitic lesions 8.Tuberculous gingival lesions 9.Candidiasis 10.Agranulocytosis and dermatoses( pemphigus and lichen planus)

15. TREATMENT PLAN: 1) 1 st visit • Goal-reduce microbial load & remove necrotic tissue • Complete evaluation of the patient • Treatment of acute lesion is primary goal. • Topical anesthetic applied • 2-3min > gently swabbed. Remove pseudo membrane and nonattached surface debris and cleaning with warm water

16. 2 nd VISIT : 2 days after the first visit Patient is evaluated for resolution of signs and Symptoms Lesion - erythematous without a superficial pseudo membrane Shrinkage of the gingiva may expose previously covered calculus, which is gently removed. Instructions are given same as previously

17. 3 RD VISIT: 5 days after the second visit - patient is evaluated for resolution of Symptoms, and a comprehensive plan for the management of the patients periodontal conditions is formulated Hydrogen peroxide rinse - discontinued Chlorhexidine mouthwash - continued 2 or3 weeks Supportive therapy ( e.g rest, appropriate fluid intake, soft nutritious diet )