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Induced Gingival Diseases

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Induced Gingival Diseases Received: 9 March 2017 | Revised: 4 September 2017 | Accepted: 13 September 2017 DOI: 10.1111/jcpe.12938 2017 WORLD WORKSHOP Non–plaque‐induced gingival diseases Palle Holmstrup1 | Jacqueline Plemons2 | Joerg Meyle3 1Section of Periodontology, Department of Odontology, Faculty of Health and Medical Abstract Sciences, University of Copenhagen, While plaque‐induced gingivitis is one of the most common human inflammatory dis‐ Copenhagen, Denmark eases, several non–plaque‐induced gingival diseases are less common but often of 2Department of Periodontics, Texas A&M University College of Dentistry, Dallas, TX, major significance for patients. The non–plaque‐induced gingival lesions are often USA manifestations of systemic conditions, but they may also represent pathologic 3Department of Periodontology, University changes limited to gingival tissues. A classification is proposed, based on the etiology of Giessen, Giessen, Germany of the lesions and includes: Genetic/Developmental disorders; Specific infections; Correspondence Inflammatory and immune conditions and lesions; Reactive processes; Neoplasms; Prof. Palle Holmstrup, Section of Periodontology, Department of Odontology, Endocrine, Nutritional and metabolic diseases; Traumatic lesions; and Gingival Faculty of Health and Medical Sciences, pigmentation. University of Copenhagen, 20 Noerre Allé, DK‐2200 Copenhagen, Denmark. Email: [email protected] KEYWORDS classification, diagnosis oral, epulis, gingiva, gingival diseases, immunological, inflammation, The proceedings of the workshop were mouth mucosa, oral manifestations, oral medicine, periodontal disease, rare diseases jointly and simultaneously published in the Journal of Periodontology and Journal of Clinical Periodontology. Human gingiva as well as other oral tissues may exhibit several non– and to discuss briefly the more common of these. The major differ‐ plaque‐induced pathologic lesions, which may in some instances be ence between the present classification proposal and that of the manifestations of a systemic condition or a medical disorder. They may 1999 workshop is creation of a more comprehensive nomenclature also represent pathologic changes limited to gingival tissues. Although and inclusion of ICD‐10 diagnostic codes. Because some of the con‐ these lesions are not directly caused by plaque, their clinical course ditions seldom manifest in the oral cavity and some even more sel‐ may be impacted by plaque accumulation and subsequent gingival in‐ dom present gingival manifestations, detailed appraisal is included flammation. Dentists are the key healthcare providers in establishing within Table 2. diagnoses and formulating treatment plans for patients affected by such lesions. Specialists in periodontology should be familiar with and DESCRIPTION OF SELECTED DISEASE be able to diagnose, treat, or refer for treatment any such lesion. ENTITIES: A review of non–plaque‐induced gingival lesions was pre‐ sented at the 1999 International Workshop for a Classification of 1 | GENETIC/DEVELOPMENTAL Periodontal Diseases and Conditions,1 and the present review aims ABNORMALITIES to add available additional literature as well as diseases and condi‐ tions which were not included in the former review. Several of the 1.1 | Hereditary gingival fibromatosis (HGF) diseases and their treatment have been reviewed recently.2‒4 The purpose of the current review is not to repeat the details of such Clinically, gingival fibromatosis may present gingival overgrowth in texts, but to present a contemporary classification of the most rele‐ various degrees. Compared to drug‐related gingival overgrowth, he‐ vant non–plaque‐induced gingival diseases and conditions (Table 1) reditary gingival fibromatosis is a rare disease which may occur as © 2018 American Academy of Periodontology and European Federation of Periodontology S28 | wileyonlinelibrary.com/journal/jcpe J Clin Periodontol. 2018;45(Suppl 20):S28–S43. HOLMSTRUP ET AL. | S29 TABLE 1 Classification table summary: non–plaque‐induced an isolated disease or as part of a syndrome. It has a genetic basis in gingival diseases and conditions mutations of the Son of Sevenless gene5 (see Table 2). 1 Genetic/developmental disorders 1.1 Hereditary gingival fibromatosis (HGF) 2 Specific infections 2 | SPECIFIC INFECTIONS 2.1 Bacterial origin Necrotizing periodontal diseases (Treponema spp., Selenomonas spp., Fusobacterium spp., Prevotella intermedia, and others) 2.1 | Bacterial origin Neisseria gonorrhoeae (gonorrhea) Treponema pallidum (syphilis) Mycobacterium tuberculosis (tuberculosis) Necrotizing periodontal disease Streptococcal gingivitis (strains of streptococcus) 2.2 Viral origin Necrotizing gingivitis (NG), necrotizing periodontitis (NP), and Coxsackie virus (hand‐foot‐and‐mouth disease) necrotizing stomatitis (NS) are severe inflammatory periodontal Herpes simplex 1/2 (primary or recurrent) diseases caused by bacterial infection in patients with specific un‐ Varicella‐zoster virus (chicken pox or shingles affecting V nerve) Molluscum contagiosum virus derlying risk factors (poor oral hygiene, smoking, stress, poor nutri‐ Human papilloma virus (squamous cell papilloma, condyloma tion, compromised immune status [e.g., HIV]). acuminatum, verrucca vulgaris, and focal epithelial hyperplasia) 2.3 Fungal Although the necrotizing diseases often run an acute, rapidly de‐ Candidosis structive course, the term acute has not been included in the diag‐ Other mycoses (e.g., histoplasmosis, aspergillosis) noses since 1999. Since superficial necrosis always involves an ulcer, 3 Inflammatory and immune conditions and lesions 3.1 Hypersensitivity reactions it is requested to delete the term “ulcerative.” The term “gingivitis” Contact allergy is used for lesions only involving gingival tissue and characterized by Plasma cell gingivitis 6 Erythema multiforme no loss of periodontal attachment. Central necrosis of the papillae 3.2 Autoimmune diseases of skin and mucous membranes may result in considerable tissue destruction with formation of a cra‐ Pemphigus vulgaris ter. If loss of attachment is established, the diagnosis consequently Pemphigoid 7 Lichen planus becomes NP. For lesions with ulceration extending >1.0 cm from the Lupus erythematosus gingival margin, including tissue beyond the mucogingival junction, 3.3. Granulomatous inflammatory conditions (orofacial granulomatosis) 8 Crohn's disease the term NS has been used. The three necrotizing diseases appear Sarcoidosis to represent various stages of the same disease process,9 and a dis‐ 4 Reactive processes tinction between the different manifestations has not always been 4.1 Epulides Fibrous epulis made in the literature. As a result, the term “necrotizing periodontal Calcifying fibroblastic granuloma disease” (NPD) is proposed as a common term encompassing NG, Pyogenic granuloma (vascular epulis) Peripheral giant cell granuloma (or central) NP, and NS. Further details are presented in Table 2. A constant and 5 Neoplasms variable part of the microflora in NPD lesions have been described. 5.1 Premalignant The constant flora primarily contains Treponema spp., Selenomonas Leukoplakia Erythroplakia spp., Fusobacterium spp., and Prevotella intermedia; the variable flora 5.2 Malignant consists of a heterogeneous array of bacterial types.10,11 Squamous cell carcinoma Leukemia Lymphoma 6 Endocrine, nutritional, and metabolic diseases Other bacterial infections 6.1 Vitamin deficiencies Vitamin C deficiency (scurvy) Non–plaque‐associated bacterial infections of the gingiva are un‐ 7 Traumatic lesions common. Gingivitis caused by a specific bacterial infection may, 7.1 Physical/mechanical insults Frictional keratosis however, arise due to a loss of homeostasis between non–plaque‐ Toothbrushing‐induced gingival ulceration related pathogens and innate host resistance.12 Acute streptococcal Factitious injury (self‐harm) gingivitis is an example of a rare acute non–plaque‐associated gin‐ 7.2 Chemical (toxic) insults 13‒15 Etching gival inflammation. Other examples of specific bacterial infec‐ Chlorhexidine tions of the gingiva may also be due to Neisseria gonorrhoeae16,17 and Acetylsalicylic acid 12,16‒18 Cocaine Treponema pallidum. Orofacial tuberculosis is a rare manifes‐ Hydrogen peroxide tation of extrapulmonary tuberculosis, occurring in approximately Dentifrice detergents 0.1% to 5% of all tuberculosis infections.19 Paraformaldehyde or calcium hydroxide 7.3 Thermal insults Burns of mucosa 8 Gingival pigmentation 2.2 | Viral origin Gingival pigmentation/melanoplakia Smoker's melanosis The most important viruses to cause gingival manifestations are Drug‐induced pigmentation (antimalarials; minocycline) Coxsackie viruses and the herpes viruses including herpes simplex Amalgam tattoo virus types 1 (HSV‐1) and 2 (HSV‐2) and varicella‐zoster virus.20 S30 | HOLMSTRUP ET AL. Although these viruses most often infect individuals in childhood, skin. In adults, the disease appears in the genital areas and is often primary infections may occur in adult life as well. They may give rise sexually transmitted. to oral mucosal disease followed by periods of latency and some‐ times reactivation. Human papilloma virus (HPV) More than 100 types of HPV have been identified, and at least the Coxsackie viruses following 25 types have been detected in oral lesions: 1, 2, 3, 4, 6, 7, Coxsackie viruses may cause herpangina and hand‐foot‐and‐mouth 10, 11, 13, 16, 18, 31, 32, 33, 35, 40, 45, 52, 55, 57, 58, 59, 69, 72, 73. disease (synonym: vesicular stomatitis with exanthema). While her‐
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