Acute necrotizing ulcerative gingivitis.

Acute necrotizing ulcerative gingivitis is a kind of acute gingival infection

1. ANUG DR AKANKSHA SINGH SENIOR LECTURER DEPTT OF PERIODONTOLOGY AND ORAL IMPLANTOLOGY ITS CDSR, GHAZIABAD DATE- 07.09.24 DR.NAYAN MDS 1 ST YEAR

2. OBJECTIVE To review the etiology of necrotizing gingival diseases. Describe the presentation of a patient with necrotizing gingival diseases. Summarize the management of a patient with NUG.

3. CONTENTS Introduction Signs and Symptoms Clinical Course Histopathology Diagnosis Differential Diagnosis Etiology Management Conclusion References Suggested reading Frequently asked questions

4. INTRODUCTION Acute Necrotizing ulcerative gingivitis (ANUG) is a severe inflammatory disease of the gingiva caused by bacteria that most often occurs in an impaired host with risk factors (e.g., poor oral hygiene, smoking, poor nutrition, compromised immune system).

5. Historically, NUG has been identified as an acute disease. Although the acronym ANUG (acute necrotizing ulcerative gingivitis) is frequently used, it is a misnomer. However, the term acute is used as a clinical descriptor rather than a diagnostic term because chronic forms of the disease do not exist. The term acute has not been used in diagnosis since 1999

6. CLASSIFICATION   1986- Necrotizing ulcerative gingivoperiodontitis 1989 – NUP ( World workshop of Clinical Periodontics ) 1999 – Classification of Periodontal Diseases – NUG & NUP , included under the broader classification of Necrotizing Ulcerative Periodontal Disease 2017 Classification :Periodontitis: Necrotizing Periodontal Diseases

7. SYNONYMS Ulceromembranous gingivitis Trench mouth (Pickard 1973) Vincent’s gingivostomatitis Phagedenic gingivitis Fusospirallary periodontitis Plaut -Vincent stomatitis

8. ORAL SIGNS AND SYMPTOMS NUG is characterized by a sudden onset of symptoms, sometimes occurring after an episode of debilitating disease or acute respiratory tract infection. Spontaneous gingival hemorrhage and pronounced bleeding after the slightest stimulation are characteristic clinical signs. Fetid odor and increased salivation are also common characteristics of NUG

9. Characteristic lesions are punched-out, craterlike depressions at the crest of the interdental papillae that subsequently extend to the marginal gingiva and rarely to the attached gingiva and oral mucosa . The lesions are extremely sensitive to touch , and the patient often complains of a constant radiating, gnawing pain that is intensified by spicy or hot foods and chewing . There is a foul metallic taste, and the patient is conscious of an excessive amount of pasty saliva.

10. EXTRAORAL AND SYSTEMIC SIGNS AND SYMPTOMS Local lymphadenopathy and a slight elevation in temperature are common features of the mild and moderate stages of the disease. In severe cases, patients may present with high fever, increased pulse rate, leukocytosis, loss of appetite, and general lassitude.

11. Systemic reactions are more severe in children. Insomnia, constipation, gastrointestinal disorders, headache, and mental depression sometimes accompany the condition. In rare cases, severe sequelae, such as gangrenous stomatitis have been described.

12. CLINICAL COURSE The clinical course varies among individuals. The severity of NUG often diminishes without treatment, leading to a subacute stage with milder clinical symptoms. Some patients experience repeated remissions and exacerbations, and the condition can recur in previously treated patients. If untreated, especially in an immunocompromised host, NUG can lead to progressive destruction of the periodontium and gingival recession accompanied by an increase in the severity of systemic complications

13. HISTOPATHOLOGY At the microscopic level, NUG is a nonspecific, acute necrotizing inflammation of the gingival margin that involves the stratified squamous epithelium and the underlying connective tissue. Comparable microscopic changes result from trauma, chemical irritation, or the application of caustic medications.

14. The surface epithelium is destroyed, and replaced by a meshwork of fibrin, necrotic epithelial cells, polymorphonuclear leukocytes (PMNs, predominantly neutrophils), and various types of microorganisms. At the immediate border of the necrotic pseudomembrane, the epithelium is edematous, and the individual cells exhibit various degrees of hydropic degeneration. PMNs infiltrate the intercellular spaces.

15. The underlying connective tissue is markedly hyperemic, with numerous engorged capillaries and a dense infiltration of PMNs. This acutely inflamed zone appears clinically as the linear erythema beneath the surface pseudomembrane. Numerous plasma cells can appear in the periphery of the infiltrate; this is interpreted as an area of established gingivitis on which the acute lesion became superimposed. The epithelium and connective tissue alterations diminish with distance from the necrotic gingival margin, blending gradually with the uninvolved gingiva.

16. RELATIONSHIP OF BACTERIA AND ANUG LESION Light microscopy shows that the exudate on the surface of the necrotic lesions contains microorganisms that morphologically resemble cocci, fusiform bacilli, and spirochetes. The layer between the necrotic and living tissue contains enormous numbers of fusiform bacilli and spirochetes in addition to leukocytes and fibrin.

17. Spirochetes and other bacteria invade the underlying living tissue. Most spirochetes occur in non-necrotic tissue before other types of bacteria, and they can achieve high-intercellular concentrations in the epithelium and connective tissue adjacent to the ulcerated lesion.

18. DIAGNOSIS Diagnosis is based on clinical findings of gingival pain, ulceration, and bleeding. A bacterial smear is not necessary or definitive because the bacterial picture is not appreciably different from that of patients with marginal gingivitis, periodontal pockets, pericoronitis, or primary herpetic gingivostomatitis.

19. Malek R, Gharibi A, Khlil N, Kissa J. Necrotizing ulcerative gingivitis. Contemp Clin Dent 2017;8:496-500

20. DIFFERENTIAL DIAGNOSIS NUG should be differentiated from other conditions that resemble it in some respects. Treatment options for these diseases vary dramatically, and misdiagnosis and improper treatment can exacerbate the condition.

21. ETIOLOGY 1. Role of Bacteria: Plaut in 1894 and Vincent in 1896 postulated that NUG was caused by specific bacteria: fusiform bacilli and spirochetal organisms. Several observations support this concept, including that spirochetal organisms and fusiform bacilli are always found in patients with the disease along with other organisms.

22. Rosebury and colleagues described a fusospirochetal complex that consists of T. microdentium, intermediate spirochetes, vibrios, fusiform bacilli, and filamentous organisms in addition to several Borrelia species . Loesche and colleagues described a predominant constant flora and a variable flora associated with NUG. The constant flora is composed of Prevotella intermedia in addition to the Fusobacterium, Treponema, and Selenomonas species. The variable flora consists of a heterogeneous array of bacterial types.

23. 2. Role of the Host Response: In the early descriptions of the disease, NUG was associated with physical and emotional stress and decreased resistance to infection. Regardless of whether specific bacteria are implicated in the cause of NUG, the presence of these organisms without other predisposing factors appears to be insufficient to cause the disease.

24. 3. Local Predisposing Factors: Preexisting gingivitis, injury to the gingiva, and smoking are important predisposing factors. Although NUG can appear in an otherwise disease-free mouth, it most often occurs superimposed on preexisting gingival disease and periodontal pockets. Deep periodontal pockets and pericoronal flaps are particularly vulnerable areas because they offer a favorable environment for the proliferation of anaerobic fusiform bacilli and spirochetes.

25. Areas of the gingiva that are traumatized by opposing teeth in malocclusion (e.g., palatal surface behind the maxillary incisors, labial gingival surface of the mandibular incisors) can predispose the area to development of NUG in a susceptible individual. Pindborg reported that 98% of his patients with NUG were smokers and that the increasing frequency of this disease correlates with increasing exposure to tobacco smoke.

26. 4. Systemic Predisposing Factors: NUG is not found in well-nourished individuals with a fully functional immune system. It is therefore important for the clinician to determine the predisposing factors for immunodeficiency. Immunodeficiency can be related to nutritional deficiency, psychosocial stress, fatigue caused by chronic sleep deficiency, other health impairing habits (e.g., alcoholism, drug abuse), and systemic disease (e.g., diabetes, debilitating infection).

27. 5. Nutritional Deficiency: Necrotizing gingivitis has been produced in animals by giving them nutritionally deficient diets. Several researchers found an increase in the fusospirochetal flora in the mouths of the experimental animals, but the bacteria were regarded as opportunists that proliferated only when the tissues were altered by the deficiency.

28. 6. Debilitating Disease: Debilitating systemic disease can predispose patients to NUG. Systemic disturbances include chronic diseases (e.g., syphilis, cancer), severe gastrointestinal disorders (e.g., ulcerative colitis), blood dyscrasias (e.g., leukemia, anemia), and AIDS. Nutritional deficiency that results from debilitating disease can be an additional predisposing factor.

29. 7. Psychosomatic Factors: Psychological factors appear to be important in the cause of NUG. The disease often occurs in association with stressful situations (e.g., induction into the armed forces, academic examinations).

30. Psychological disturbances and increased adrenocortical secretion are common in patients with the disease. It can be concluded that opportunistic bacteria are the primary etiologic agents of NUG in patients who demonstrate immunosuppression. Stress, smoking, and preexisting gingivitis are common predisposing factors.

31. COMMUNICABILITY NUG often occurs in groups in an epidemic pattern. At one time, it was considered contagious, and required reporting to the community health department, but it was later concluded not to be communicable. It has been demonstrated that disease associated with the fusospirochetal bacterial complex is transmissible; however, it is not communicable or contagious.

32. MANAGEMENT (1) alleviation of the acute inflammation by reduction of the microbial load, and removal of necrotic tissue, (2) treatment of chronic disease either underlying the acute involvement or elsewhere in the oral cavity, (3) alleviation of generalized symptoms, such as fever and malaise, and (4) correction of systemic conditions or factors that contribute to the initiation or progression of gingival changes.

33. Syam S, Maheswari TN. Guidelines for Clinical Management of patients with Acute Necrotizing Ulcerative Gingivitis: A Literature Review. Research Journal of Pharmacy and Technology. 2019;12(8):4027-30

34. First Visit Treatment of NUG should follow an orderly sequence, according to specific steps, at three clinical visits. On the first visit, the clinician should conduct a comprehensive evaluation of the patient, including a thorough medical history, with special attention to recent illness, living conditions, dietary background, cigarette smoking, type of employment, hours of rest, risk factors for HIV infection, and psychosocial parameters (e.g., stress, depression).

35. The initial physical examination should include an assessment of general appearance, presence of halitosis, presence of skin lesions, vital signs including temperature, and palpation for the presence of enlarged lymph nodes, especially submaxillary and submental nodes. The oral cavity is examined for the characteristic NUG lesions, distribution, and the possible involvement of the oropharyngeal region. Oral hygiene is evaluated, with special attention to the presence of peri coronal flaps, periodontal pockets, and local risk factors (e.g., poorly contoured and ill-fitting restorations, presence and distribution of calculus).

36. The goals of initial therapy are reduction of the microbial load and removal of necrotic tissue to the degree that repair and regeneration of normal tissue barriers can be reestablished. Treatment during the initial visit is confined to the acutely involved areas , which are isolated with cotton rolls and dried. A topical anesthetic is applied, and after 2 or 3 minutes, the areas are gently swabbed with a moistened cotton pellet to remove the pseudo membrane and nonattached surface debris.

37. The area is cleansed with warm water, the superficial calculus is removed. Ultrasonic scalers are very useful for this purpose because they do not elicit pain, and the water jet and cavitation aid in lavage of the area. Subgingival scaling and curettage are contraindicated as it may extend the infection into the deeper tissues and may also cause bacteremia. Unless an emergency exists, procedures such as extraction or periodontal surgery are postponed until the patient has been symptom-free for 4 weeks to minimize the likelihood of exacerbating the acute symptoms.

38. Antibiotics are effective in the treatment of patients with NUG. Patients with moderate or severe NUG and local lymphadenopathy or other systemic signs or symptoms are placed on an antibiotic regimen of amoxicillin 500 mg orally every 6 hours for 10 days . For amoxicillin-sensitive patients , other antibiotics are prescribed, such as erythromycin (500 mg every 6 hours) or metronidazole (500 mg twice daily for 7 days) . Systemic complications should subside in 1 to 3 days. Antibiotics are not recommended in NUG patients who do not have systemic complications.

39. Instructions to the Patient The patient is discharged with the following instructions: Avoid tobacco, alcohol, and condiments. Rinse with a glassful of an equal mixture of 3% hydrogen peroxide and warm water every 2 hours and/or 0.12% chlorhexidine solution twice daily.

40. 3. Get adequate rest. Pursue usual activities, but avoid excessive physical exertion or prolonged exposure to the sun. 4. Confine toothbrushing to removal of surface debris with either a bland dentifrice or just water and an ultrasoft brush. 5. An analgesic, such as a nonsteroidal anti-inflammatory drug ( NSAID ; e.g., ibuprofen), is appropriate for pain relief .

41. 6. Patients who have systemic complications, such as high fever, malaise, anorexia, or general debility, are given antibiotics and instructed to get plenty of bed rest, and drink lots of fluids. 7. Patients are asked to report back to the clinician in 1 to 2 days.

42. Second Visit The patient is evaluated for amelioration of signs and symptoms. The patient’s condition is usually improved and pain is diminished or is no longer present. The gingival margins of the involved areas are erythematous but without a superficial pseudo membrane.

43. Scaling is performed if it is necessary and if sensitivity permits. Shrinkage of the gingiva may expose previously covered calculus, which is gently removed. Instructions to the patient are the same as those given previously

44. Third Visit Approximately 5 days after the second visit, the patient is evaluated for resolution of symptoms, and a comprehensive plan for management of the patient’s periodontal condition is formulated. Some erythema may still be present in the involved areas, and the gingiva may be slightly painful on tactile stimulation. The patient is counseled on nutrition, and other conditions or habits associated with potential recurrence.

45. The hydrogen peroxide rinses are discontinued, but chlorhexidine rinses may be maintained for an additional 2 or 3 weeks. Scaling and root planing is repeated if necessary. Patients need to be educated about the importance of comprehensive periodontal treatment and encouraged to complete it.

46. Appointments should be scheduled for treatment of gingivitis, periodontal pockets, and peri coronal flaps, as well as for elimination of all forms of local risk factors. The patient should be reevaluated approximately 4 to 6 weeks after treatment to determine compliance with oral hygiene, health habits, psychosocial factors, the potential need for reconstructive or esthetic surgery, and the interval of subsequent recall visits.

47. Persistent or recurrent cases If a case of NUG persists despite therapy or if it recurs, the patient should be reevaluated with a focus on the following factors: Reassessment of differential diagnosis to rule out diseases that resemble NUG: Several diseases and conditions (e.g., desquamative gingivitis) may initially manifest with an appearance similar to that of NUG. A renewed search for skin lesions and other signs or symptoms should be undertaken, with a biopsy if warranted.

48. 2. Underlying systemic disease causing immunosuppression: In particular, HIV infection may frequently manifest with symptoms of NUG or NUP. The patient should be reassessed for risk factors and may need counseling about testing for HIV or other suspected underlying systemic diseases (e.g., lymphoproliferative disease). The patient will likely need referral to their physician for further evaluation.

49. 3. Inadequate local therapy: Too often, treatment is discontinued when the symptoms have subsided without elimination of the gingival disease and periodontal pockets that remain after the superficial acute condition is relieved. Remaining calculus and other local factors that predispose to gingival inflammation may contribute to recurrence.

50. 4. Inadequate compliance: Poor biofilm control, heavy use of tobacco, ineffective stress management, and continued malnutrition can also contribute to persistence or recurrence of NUG. The clinician should evaluate the quality and consistency of biofilm control. If the clinician perceives that unresolved psychosocial factors are complicating health, the patient should be referred to an appropriate professional.

51. REFERENCES Textbook of Carranza, 13 th edition. Albandar JM, Tinoco EM. Global epidemiology of periodontal diseases in children and young persons. Periodontol 2000 . 2002;29:153–176. Amir J, Harel L, Smetana Z, et al. Treatment of herpes simplex gingivostomatitis with aciclovir in children: a randomised double blind placebo controlled study. BMJ . 1997;314:1800–1803. Barros SP, Offenbacher S. Modifiable risk factors in periodontal disease: epigenetic regulation of gene expression in the inflammatory response. Periodontol 2000 . 2014;64:95–110. Berke JD. Experimental study of acute ulcerative stomatitis. J Am Dent Assoc . 1961;63:86–90.

52. Suggested Reading Carranza’s Clnical Periodontology;ch . Newman, Takie , Klokkevold , Carranza 10 th 9 th ,8thEdition. Acute necrotizing ulcerative gingivitis: risk factors involving host defense mechanisms.-- Yoji , Hidemi , Atsushi: Periodontology 2000, Vol. 6, 1994, 116-124. .

53. FREQUENTLY ASKED QUESTIONS Q.1 Describe the Clinical Features, signs & symptoms of NUG Q.2 Write in detail about Necrotizing Periodontal diseases Q.3 Short notes on- ANUG MANAGEMENT OF ANUG

54. Link to video https://www.youtube.com/watch?v=kr_qdMV1z7U

55. MULTIPLE CHOICE QUESTIONS 1.WHICH OF THE FOLLOWING IS NOT FOUND IN ACUTE NECROTISING ULCERATIVE GINGIVITIS? POCKET FORMATION BONE LOSS TOOTH LOSS GINGIVAL RECESSION 2.WHICH OF THE FOLLOWING CONDITIONS IF NOT TRETAED PROPERLY MAY LEAD TO NOMA? DIPTHERIA HERPENGINA ANUG HERPETIC GINGIVOSTOMATITIS

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