Non plaque induced gingivitis

presentation of Non plaque induced gingivitis

1. Non-plaque Induced G ingivitis Dr.Haddadi

2. R eference: Clinical Periodontology and Implant Dentistry, Lindhe , 2015, Chapter 18

3. Introduction: Gingivitis is not always due to accumulation of plaque on the tooth surface. They may have several causes; S pecific bacterial, viral or fungal infection, H ereditary gingival fibromatosis , Muco-cutaneous disorders (lichen planus, pemphigoid, pemphigus vulgaris, erythema multiform), Allergic and traumatic lesions.

4. Gingival diseases of specific bacterial origin Typical examples of such lesions are due to infections with Neisseria gonorrhea, Treponema pallidum , streptococci . Oral lesions may be the primary presentation of the infection. Although oral manifestations of syphilis and gonorrhea are most likely to be observed during secondary disease, all stages of the disease can give rise to oral lesions. The gingival lesions manifest as fiery red edematous painful ulcerations, as asymptomatic mucous patches, or as atypical non‐ulcerated, highly inflamed gingivitis . Diagnosis: Biopsy supplemented by microbiologic examination.

5. Oral manifestation of syphilis

6. Gingival diseases of viral origin Primary herpetic gingivostomatitis: The manifestation includes painful severe gingivitis with redness, ulcerations with serofibrinous exudate, and edema accompanied by stomatitis. The incubation period is 1 week. A characteristic feature is the formation of vesicles , which rupture, coalesce, and leave fibrincoated ulcers.

7. Fever and lymphadenopathy are other classic features. Healing occurs spontaneously without Scarring in 10–14 days. During this period pain can render eating difficult . Occurs mostly before adolescence. The virus remains latent in the ganglion cell, probably through integration of its DNA . Reactivation of the virus occurs in 20–40% of primary infected individuals, usually presents as herpes labialis, but recurrent intraoral herpes Infections are also seen.

8. Recurrent intraoral herpes typically presents a less dramatic course than does the primary infection. A characteristic manifestation is a cluster of small painful ulcers in the attached gingiva and hard palate. Diagnosis: on the basis of the patient history and clinical findings supported by isolation of HSV from lesions . Laboratory diagnosis may also involve examination of a blood sample for increased antibody titer against HSV.

9. The treatment of herpetic gingivostomatitis includes careful plaque removal to limit bacterial superinfection of the ulcerations, which delays their healing . In severe cases , including patients with immunodeficiency, the systemic use of antiviral drugs such as acyclovir, valacyclovir or famciclovir is recommended.

10. Gingival diseases of fungal origin Candidosis : The most common fungal infection of the oral mucosa is candidosis mainly caused by the organism C. albicans . C. albicans is a normal commensal of the oral cavity but also an opportunistic pathogen. The prevalence of oral carriage of C. albicans in healthy adults ranges from 3% to 48 %. The proteinase‐positive Strains of C. albicans are associated with disease and invasion of keratinized epithelia such as that of the gingiva.

11. Infection by C. albicans usually occurs as a consequence of reduced host defense, including immunodeficiency, reduced saliva secretion, smoking, t reatment with corticosteroids. Disturbances in the oral microbial flora, such as after therapy with broad‐spectrum antibiotics, may also lead to oral candidosis . The most common clinical characteristic of gingival candida infections is redness of the attached gingiva, often associated with a granular surface. (Erythematous candidosis)

12. Pseudomembranous candidosis shows whitish patches which can be wiped off the mucosa with an instrument or gauze to leave a slightly bleeding surface . The pseudomembranous type usually has no major symptoms. Diagnosis: on the basis of culture, smear, and biopsy.

13. Topical treatment involves application of antifungals, such as nystatin, amphotericin B or miconazole . Miconazole exists as an oral gel. It should not be given during pregnancy and it can interact with anticoagulants and phenytoin. Nystatin may be used as an oral suspension. Since it is not resorbed, it can be used in pregnant or lactating women . The treatment of severe or generalized forms also involves systemic antifungals such as fluconazole .

14. Gingival lesions of genetic origin Hereditary gingival fibromatosis: It is an uncommon condition characterized by diffuse gingival enlargement , sometimes covering major parts of or the entire tooth surfaces . The lesions develop irrespective of effective plaque removal .

15. Most cases are related to an autosomal dominant mode of inheritance, but cases have been described with an autosomal recessive background. The most common syndrome of HGF includes hypertrichosis , epilepsy, and mental retardation ; the latter two features, however, are not present in all cases.

16. The treatment is surgical removal, often in a series of gingivectomies, but relapses are not uncommon. If the volume of the overgrowth is extensive, a repositioned flap to avoid exposure of connective tissue by gingivectomy may better achieve elimination of pseudopockets .

17. Gingival diseases of systemic origin A variety of mucocutaneous disorders present gingival manifestations , sometimes in the form of desquamative lesions or ulceration of the gingiva.

18. Lichen planus Lichen planus is the most common mucocutaneous disease manifesting on the gingiva . The disease may affect the skin and oral as well as other mucosal membranes in some patients, while others may present with either skin or oral mucosal involvement alone . Skin lesions are characterized by papules with white striae (Wickham striae ). Itching is a common symptom, and the most frequent locations are the flexor aspects of the arms and neck.

19. Papular form Reticular form

20. Erythematous and ulcerative form Plaque type

21. The most characteristic clinical manifestations of the disease and the basis of the clinical diagnosis are white papules and white striations, usually bilaterally. Papular, reticular , and plaque‐type lesions usually do not give rise to significant symptoms, whereas erythematous and ulcerative lesions are associated with moderate to severe pain, especially in relation to oral hygiene procedures and eating. The clinical diagnosis is based on the presence of papular or reticular lesions. The diagnosis may be supported by histopathologic findings of hyperkeratosis, degenerative changes of basal cells, and subepithelial inflammation dominated by lymphocytes and macrophages.

22. When gingiva is involved, the most important part of the therapeutic regimen is atraumatic meticulous plaque control, which results in significant improvement in many patients. In painful cases who have not responded to the treatment above, topical corticosteroids, preferably in a paste or an ointment, should be used three times daily for a number of weeks.

23. Pemphigoid Pemphigoid is a group of disorders in which a utoanibodies towards components of the basement membrane result in detachment of the epithelium from the connective tissue. Bullous pemphigoid predominantly affects the skin, but oral mucosal involvement may occur. If only mucous membranes are affected, the term benign mucous membrane pemphigoid (BMMP ) is often used . The majority of affected patients are female with a mean age at onset of 50 years or ove

24. Any area of the oral mucosa may be involved in BMMP, but the main manifestation is desquamative lesions of the gingiva present in as intensely erythematous attached gingiva. Rubbing the gingiva may precipitate bulla formation. This is denoted a positive Nicholsky sign and is caused by the destroyed adhesion of the epithelium to the connective tissue .

25. Therapy consists of professional atraumatic plaque removal and individual instruction in gentle, but careful, daily plaque control, eventually supplemented with daily use of chlorhexidine and/or topical Corticosteroid application if necessary.

26. Pemphigus vulgaris: Pemphigus is a group of autoimmune diseases characterized by formation of intraepithelial bullae in skin and mucous membranes. Since the bulla formation is located in the spinous cell layer, the chance of seeing an intact bulla is even more reduced than in BMMP. The disease may occur at any age, but is typically seen in the middle aged or elderly, if left untreated the disease is life threatening.

27. Intraoral onset of the disease with bulla formation is very common and lesions of the oral mucosa, including the gingiva, are frequently seen. Early lesions may resemble aphthous ulcers. Gingival involvement may present as painful desquamative lesions or as erosions or ulcerations, which are the remains of ruptured bullae.

28. The ulcers heal slowly, usually without scar formation, and the disease runs a chronic course with recurring bulla formation. Diagnosis of PV is based on the characteristic histologic feature of intraepithelial bulla formation due to destruction of desmosomes resulting in acantholysis . Immediate referral of patients with PV to a dermatologist or internal medicine specialist is important because when recognized late, the disease can be fatal, although systemic corticosteroid therapy can presently treat most cases.

29. Erythema multiforme: Erythema multiforme (EM) is a reactive acute, sometimes recurrent , vesiculobullous disease affecting mucous membranes and skin . A general malaise often precedes the lesions. The spectrum of the disease is from a self‐limited, mild, exanthematic, cutaneous variant with minimal oral involvement to a progressive, fulminating , severe variant with extensive mucocutaneous epithelial necrosis (Stevens–Johnson syndrome).

30. The characteristic oral lesions comprise swollen lips often with extensive crust formation of the vermilion border. The basic lesions, are bullae that rupture and leave extensive ulcers, usually covered by heavy yellowish fibrinous exudates sometimes described as pseudomembranes.

31. The skin lesions are characteristic due to the iris appearance with a central bulla surrounded by a blanched halo within an erythematous zone. Although periodontal lesions are not the most frequent intraoral manifestation, they can sometimes pose a differential diagnostic problem. As for any intraoral ulcerations, gentle plaque control and professional cleaning are mandatory. The treatment often involves systemic corticosteroids, but topical treatment may be effective in cases with minor lesions .

32. Allergic reactions Oral mucosal reactions may be type I reactions ( immediate type ), which are mediated by IgE , or more often they are type IV reactions (delayed type) mediated by T cells. 1. Reactions to dental restorative materials 2. Reactions to oral hygiene products, chewing gum, and food

33. Reactions to dental restorative materials The clinical manifestation of type IV allergy ( contact allergy ) occurs after a period of 12–48 hours following contact with the allergen. Oral mucosal reactions to restorative materials include reactions to mercury, nickel, gold, zinc, chromium, palladium , and acrylics. The lesions , have clinical similarities with those for OLP, which is why they are denoted OLLs or oral leukoplakia.

34. Reactions to oral hygiene products, chewing gum, and food: The constituents responsible for the allergic reactions may be flavor additives, for instance cinnamon or preservatives. The clinical manifestations of allergy include a diffuse, fiery red edematous gingivitis, sometimes with ulcerations or whitening.

35. Any question..?