Necrotizing Ulcerative Gingivitis

1. Necrotizing Ulcerative Gingivitis Necrotizing ulcerative gingivitis can be defined as an acute , and sometimes recurring gingival infection of complex etiology . Characterized by rapid onset of gingival pain, interdental gingival necrosis , and bleeding .

2. Necrotizing ulcerative gingivitis has been called many names:-Vincent’s disease- Trench mouth-Acute necrotizing ulcerative gingivitis- Fusospirochetal gingivitis

3. The patients affected are typically adolescents or young adults, may be cigarettes smokers, and are often psychologically stressed.

4. During world II up to 14% of the Danish military personnel encountered NPD. Also civilians suffered from the disease

5. After world war II the prevalence of NPD declined substantially and in industrialized countries NPD it is now rare

6. Clinical signs “NUG” Pain Ulceration Necrosis of the interdental papillae Bleeding either spontaneous or to gentle manipulation.

7. Necrotizing gingivitis is an inflammatory destructive gingival condition , characterized by ulcerated and necrotic papillae and gingival margins resulting in a characteristic punched out appearance

8. The ulcers are covered by a yellowish – white or grayish slough which is termed “Pseudo membrane “

9. The sloughed material has no coherence , and bears little resemblance to a membrane.It consists primarily of fibrin and necrotic tissue with Leucocytes, erythrocytes and masses of bacteria

10. Removing of the sloughed material results bleeding and ulcerated underlying tissue becomes exposed

11. The necrotizing lesions develop rapidly and are painful , but in the initial stages , when the necrotic areas are relatively few and small , pain is usually moderate.Severe pain is often the chief reason for the patient to seek treatment

12. Bleeding is readily provoked .And may start spontaneously as well as in response to even gentle touch.

13. In early phases of the disease lesions are typically confined to the top of a few interdental papillae

14. The first lesions are often seen interproximally in the mandibular anterior region .But they may occur in any interproximal space

15. In regions where lesions first appear , there are usually also signs of preexisting chronic gingivitis , but the papillae are not always edematous at this stage .

16. The zone between the marginal necrosis and the relatively unaffected gingiva usually exhibits a well demarcated narrow erythematous zone

17. This is an expression of hyperemia due to dilation of the vessels in the gingival connective tissue in the periphery of the necrotic lesions

18. Acute necrotizing ulcerative gingivitis; typical lesions with progressive tissue destruction

19. Acute necrotizing ulcerative gingivitis: typical lesions with spontaneous hemorrhage

20. Acute necrotizing ulcerative gingivitis: typical lesions have produced irregular gingival contour.

21. Involvement of Alveolar Mucosa When the necrotic progresses beyond the mucogingival junction the condition is donated Necrotizing Stomatitis (NS) The disease is related to compromised immune functions , and malnutrition

22. Differential diagnosis of NUG is that from primary herpetic gingivostomatitis

23. NUG Etiology: Bacteria Age: 15-30 years Site: Interdental papillae Symptoms: Ulceration and necrotic tissue and a yellowish-white Duration:1-2 days if treated Contagious: No Immunity: No Healing: Destruction of periodontal tissue remain. PHGS Etiology: Herpes simplex virus Age : Frequently children Site: Gingiva and entire mucosa Symptoms: Multiple vesicles which burst leaving small round fibrin-covered ulcers which tend to coalesce. Duration: 1-2 weeks Contagious: Yes Immunity: Partial Healing: No permanent destruction Differential Diagnosis

24. AHGS

25. Swelling of Lymph Nodes Swelling of regional lymph nodes may occur in NPD is particularly evident in advanced cases. Such symptoms are usually confined to the submandibular lymph nodes , but the cervical lymph nodes may also be involved. In children with NPD , swelling of lymph nodes and increased bleeding tendency are often the most pronounced clinical findings

26. Fever and Malaise Fever and malaise is not a consistent characteristic of NPD. Some investigations indicate that elevated body temperature is not common in NG and when present the elevation of body temperature is usually moderate. The disagreement on this point may , in fact be due to misdiagnosis of primary herpetic gingivostomatitis

27. Histopathology Necrotizing gingivitis are characterized by ulceration with necrosis of epithelium and superficial layers of the connective tissue An important aspect is the role of the microorganisms in the lesion , because they have been demonstrated not only in the necrotic tissue components but also in vital epithelium and connective tissue

28. The surface cover of yellowish – white or grayish sloughthe tissue is infiltrated by large and medium sized spirochetes , but no other microorganisms have been seen

29. In the vital connective tissue the vessels are dilated. They also proliferate to form granulation tissue , and the tissue is heavily infiltrated by leucocytes.In acute processes the inflammatory infiltrate is dominated by Neutrophils , in the deeper tissue the inflammatory process comprises large numbers of monocytes and plasma cells

30. Oral Hygiene The oral hygiene in patients with NPD is usually poor . Moreover , brushing of teeth and contact with the acutely inflamed gingiva is painful . Therefore , large amounts of plaque on the teeth are common , especially along the gingival margin . A thin , whitish film sometimes covers parts of the attached gingiva. This film is a characteristic finding in patients who have neither eaten nor performed oral hygiene for days, it is composed of desquamated epithelial cells and bacteria , it is easily removable

31. Treatment The treatment of the necrotizing periodontal diseases is divided into two phases : • Acute • Maintenance

32. Acute Phase Treatment The aim of the acute phase treatment is to eliminate disease activity as manifest by ongoing tissue necrosis developing laterally and apically. A further aim is to avoid pain and general discomfort which may severely compromise food intake

33. The first consultation scaling should be attempted as thorough as the condition allows.Ultrasonic scaling may be preferable, with minimal pressure against the soft tissues , ultrasonic cleaning may accomplish the removal of soft and mineralized deposits

34. Patients should be instructed in substituting tooth brushing with chemical plaque control in such areas until healing is accomplished

35. Hydrogen peroxide and other oxygen – releasing agents also have a long standing tradition in the initial treatment o NPD.The favorable effect of hydrogen peroxide is mechanical cleaning and the influence on anaerobic bacterial flora of the liberated oxygen

36. Twice daily rinses with 0.2% chlorhexidine solution to reduce plaque formation, particularly when tooth brushing is not performed

37. In some cases of NPD the patient response to debridement is minimal or the general health is affected to such an extent that the supplementary use of systemic antibiotics

38. Supplementary Treatment • Metronidazole 250mg three times daily is the first choice in the treatment of NPD • Penicillin 500mg three times daily • Tetracycline also effective • Topical application of antibiotics is not indicated in the treatment of NPD is not indicated

39. Non – Plaque Induced Inflammatory Gingival Lesions Gingival inflammation , clinically presenting as gingivitis , is not always due to accumulation of plaque on the tooth surface , and non plaque induced inflammatory gingival reactions often present characteristic clinical features

40. They may occur due several causes , such as specific bacterial , viral , or fungal infection without an associated plaque related gingival inflammatory reaction

41. Gingival lesions of genetic origin are seen in hereditary gingival fibromatosis , and several mucocutaneous disorders manifest as gingival inflammation ( Lichen planus , pemphigoid , pemphigus vulgaris and erythema multiforme )

42. Gingival Diseases Of Specific Bacterial Origin Infective gingivitis and Stomatitis may occur on rare occasions in both immunocompromised and non – immunocompromised individuals Necrotizing Stomatitis in mandibular left molar area

43. This lesions are due to infections with:-Neisseria gonorrhea-Treponema pallidum-Streptococci-Mycobacterium chelonae

44. The gingival lesions manifest Fiery red edematous painful ulcerations Asymptomatic chancres or mucous patches Highly inflamed gingivitis Biopsy supplemented by microbiologic examination reveals the background of the lesions

45. Acute herpetic gingivostomatitis vesicles on the gingiva Acute herpetic gingivostomatitis typical diffuse erythema

46. Gingival Diseases Of Viral Origin A number of viral infections are known to cause gingivitis . The most important are herpes viruses. 1) Herpes simplex viruses type 1. 2) Herpes simplex viruses type 2 3) Varicella zoster virus

47. These viruses usually enter the human body in childhood and may give rise to oral mucosal disease followed by periods of latency and sometimes reactivation

48. Herpes simplex virus type 1 usually causes oral manifestations

49. Herpes simplex virus type 2 is mainly involved in anogenital infections and only occasionally is involved in oral infection

50. Treatment Of Herpetic Gingivostomatitis Treatment includes careful plaque removal to limit bacterial super infection of the ulcerations , which delay their healing. In severe cases , including patients with immunodeficiency , the systemic use of antiviral drugs such as Acyclovir or Valacyclovir is recommended