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    GingivalEnlargement

    Malik Hudieb, BDS, PhD

    Department of Preventive Dentistry

    Faculty of Dentistry

    Jordan University of Science and Technology

    Gingival Enlargement(etiology)

    I. Inflammatory enlargement

    II. Drug induced gingival enlargement

    III. Enlargements associated with systemic disease

    IV. Neoplastic enlargement (gingival tumors)V. False enlargement

    Gingival Enlargement(location)

    1. Localized: single tooth or a group of teeth.

    2. Generalized: gingiva throughout the mouth.

    3. Marginal: Confined to the marginal gingiva.4. Papillary: Confined to the interdental papilla.

    5. Diffuse: the marginal, attached and papillae.

    6.Discrete: isolated sessile or pedunculated tumorlike enlargement.

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    SCORING OF GINGIVAL ENLARGEMENT

    Grade 0 : No signs of gingival enlargement

    Grade I : confined to interdental papilla

    Grade II : involves papilla and marginal gingiva

    Grade III : covers three quarters or more of thecrown.

    Gingival EnlargementI. Inflammatory enlargement

    A. Chronic

    B. Acute

    Copyright 2011 WoltersKluwerHealth| Lippincott Williams & Wilkins

    Gingival Enlargement

    I. Inflammatory enlargement

    A. Chronic:

    prolonged exposure

    to dental plaque

    anatomicabnormalities,improper restorativeand orthodontic

    appliances.

    Gingival Enlargement

    I. Inflammatory enlargement

    A. Chronic:

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    Gingival EnlargementI. Inflammatory enlargement

    A. Chronic:

    Usually painless and progresses slowly

    Histopathologic features:

    inflammatory cells and fluids with vascularengorgement.

    fibroblasts, collagen fibers and new capillaries inthe connective tissue.

    Gingival EnlargementI. Inflammatory enlargement

    B. Acute: Gingival Abscess:

    A localized, painful, rapidlyexpanding lesion that isusually of sudden onset.

    It is generally limited to themarginal gingiva or

    interdental papilla.

    Gingival Abscess

    Periodontally healthy mouth

    Foreign object is forced into a healthy sulcus. Limited to gingival margin

    Localized Painful swelling

    Purulent exudate may be present

    Gingival Abscess

    Involves the marginal gingiva or interdentalpapilla

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    Gingival Abscess

    Involves the marginal gingiva or interdentalpapilla

    Gingival Abscess Treatment

    Elimination of foreign object

    Drainage through sulcus withprobe or light scaling

    Control of discomfort

    Follow-up after 24-48 hours

    Recommend warm salinerinses

    Gingival Enlargement(etiology)

    I. Inflammatory enlargement

    II. Drug induced gingival enlargement

    III. Enlargements associated with systemic disease

    IV. Neoplastic enlargement (gingival tumors)

    V. False enlargement

    II. Drug induced gingival enlargement

    Importance of Medical History..

    Ask twice ..

    Medications..

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    II. Drug induced gingival enlargement

    Mostly related to enlarged interdental papillaewhich coalesce. Hereditary enlargementinvolves the entire gingiva.

    May compromise esthetics, function and impairadequate oral hygiene.

    II. Drug induced gingival enlargement

    Clinical Features:

    Initially the growth is painless,

    starts at the interdental

    papilla and extends

    to the facial and

    lingual gingivalmargins

    Copyright 2011 WoltersKluwerHealth| Lippincott Williams & Wilkins

    Clinical Features:

    The marginal andpapillary

    enlargements uniteand cover aconsiderable portionof the crowns, whichinterfere withocclusion.

    II. Drug induced gingival enlargement

    Anterior regions

    Interdental papilla

    II. Drug induced gingival enlargement

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    II. Drug induced gingival enlargement

    3 major groups (according to therapeutic action):

    1. Anticonvulsants (anti-epilyptics).

    2. Immunosuppressants.

    3. Calcium channel blockers (anti-hypertensive drugs).

    II. Drug induced gingival enlargement

    Anticonvulsant drugs:

    Phenytoin, Phenobarbital, Carbamazepine,Sodium Valproate, Primidone and Felbamate.

    Antihypertensive drugs:

    Nifedipine, Amlodipine, Nimodipine, Nicardine,Nitrendipine, Diltiazem, Felodipine and Bepridil.

    These medications modifyfibroblast function, either directly

    or indirectly through altering levels

    of cytokines/MMP activity withinthe tissue and Calcium ions influx

    to the cells.

    II. Drug induced gingival enlargement

    Phenytoin

    Fibroblasts show increased synthesis

    of sulfated glycosaminoglycans GAG.

    Decrease in collagen degradation(inactive fibroblast collagenase)

    II. Drug induced gingival enlargement

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    Role of Dental Plaque Emphasized in Armitage classification (1999):Gingival disease

    A: Dental plaque-induced gingival disease

    3. Gingival disease modified by medications

    a) drug-induced gingival diseases

    1) drug-influenced gingival enlargements

    2) drug-influenced gingivitis

    a. oral contraceptive-associated gingivitisb. other

    AAP

    1999

    Role of Dental Plaque

    Relationship between plaque and drug induced

    gingival overgrowth raises the chicken or eggfirst question.

    enlarged tissue itself does not bleed, it aidsplaque accumulation by preventing adequateoral hygiene, thus leading to gingivalinflammation (Glickman & Lewitus 1941,Seymour et al1996, Darby 2006).

    Role of Dental Plaque

    with poor oral hygiene had greater severity of

    gingival overgrowth than those with good oralhygiene (Panuska et al.1961) .

    Thomason et al(1993) and Ciancio et al(1972)also found an association between the two.

    Barclay et al(1992) found gingival changes innifedipine patients were not related to drugdosage or plaque scores.

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    Clinical presentation Gingival overgrowth normally begins at the

    interdental papillae and is frequently found in theanterior segment of the labial surfaces (Darby2006).

    Clinical manifestation usually appears within 1 to3 months after initiation of treatment with themedications (AAP 2004). For patients on

    cyclosporin, significant overgrowth wascommonly observed between 3 and 6 months(Seymour et al1987).

    Clinical presentation The fibrotic enlargement normally is

    confined to the attached gingiva but mayextend coronally and interfere withaesthetics, mastication, or speech.

    Does not necessarily altering the

    underlying periodontium.

    Clinical presentation

    Cyclosporin induced gingival overgrowth

    pebbly or papillary lesions which appear onthe surface of larger lobulations (Marshall andBartold 1999).

    Nifedipine induced gingival overgrowthgeneralized lobulated enlargement of the facialand lingual gingiva, with the nodular growthsoriginating interdentally and extending acrossthe tooth surfaces (Lederman et al1984).

    Phenytoin

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    Cyclosporin .. Niphedipine..

    Verapamil.. Felodipine

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    Pathogenesis no definitive explanation .

    Not all patients taking phenytoin,cyclosporin and/or nifedipine developgingival overgrowth (Seymour et al1996).

    gingival overgrowth is rarely observed on

    edentulous alveolar crests (Badar et al1998)

    Effect of drug dosage Conflicting studies on the effect of

    increasing dosage on the degree ofovergrowth.

    Combination of drugs

    Combination of drugs:Synergistic effect(Thomason et al1993 & 1996, Slavin &Taylor 1987). A significant increase in theincidence of gingival overgrowth has beendescribed in renal transplant patientstaking nifedipine as well as cyclosporinecompared with those taking cyclosporinalone (48% compared to 30%) (Thomasonet al1993)

    Duration of use

    Increased duration of phenytoin (Panuska etal1961) or cyclosporin (Thomason et al1996)resulted in more gingival overgrowth

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    Individual SusceptibilityInfluenced by:

    Age.

    Gender.

    Genetics.

    Age Children and adolescents appear more

    susceptible than adults (Seymour et al1996,Thomason et al1996, Darby 2006).

    However, these studies are limited to both

    phenytoin and cyclosporin that are morecommonly prescribed in this younger agegroup.

    Treatment

    Four steps:

    Drug substitution.

    Oral Hygiene.

    Antibiotics.

    Surgical intervention.

    Treatment-Drug substitution

    NOT MY WORK.. PLEASE

    CONSULTPATIENTPHYSICIAN!

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    Treatment-Oral Hygiene Reduces the inflammatory component.

    Better surgical field.

    Consider use of Chlorhexidine mouthrinseor gel.

    Usually does not result in complete

    resolution.

    Treatment- Antibiotics Conflicting reports.

    Cant depend on their use.

    May resolve the inflammatory component.

    Treatment-Surgical intervention

    External bevel or internal bevel incisions.

    Laser. CO2 Mostly for esthetic purposes, sometimes to

    facilitate oral hygiene.

    No difference between the outcome ofdifferent modalities in 6months Mavrogianniset al (2006)

    Treatment-Surgical intervention

    Recurrence if patient still on medication.Recurrence rate with cyclosporin andnefidipine is 40% within 18 months after

    active treatment (AAP 2004).

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    False enlargementsIncrease in size of the underlying osseous ordental tissues :

    Bone:

    Normal: tori, exostoses ,

    Disease: fibrous dysplasia, cherubism, centralgiant cell granuloma, ameloblastoma, osteoma,and osteosarcoma.

    False enlargements

    False enlargements

    Increase in size of the underlying osseous ordental tissues :

    Underlying Dental Tissues

    During the various stages of eruption