12 Gingival Enlargement - Dr. Dhwanit Thakore

Gingival Enlargement

Dr . Dhwanit Thakore

Introduction

Hi Doc, I am Julia……

Hyperplasia…….

Hypertrophy…….

Overgrowth…….

Enlargement……

Classification

I. Inflammatory enlargementA. ChronicB. Acute

II. Drug-induced enlargement

III. Enlargements associated with systemic diseases A. Conditioned enlargement

1. Pregnancy2. Puberty3. Vitamin C deficiency4. Plasma cell gingivitis5. Nonspecific conditioned enlargement (granuloma pyogenicum)

B. Systemic diseases causing gingival enlargement1. Leukemia2.Granulomatous diseases (Wegener's granulomatosis, sarcoidosis, and so on)

IV. Neoplastic enlargement (gingival tumors)A. Benign tumorsB. Malignant tumorsV. False enlargement

• Based on location and distribution– Localized– Generalized– Marginal – Papillary – Diffuse– Discrete

Shaefer’s classification• Inflammatory gingival hyperplasia • Non inflammatory (fibrous) gingival hyperplasia• Combination of inflammatory and fibrous hyperplasia

Scoring

• Grade 0: No signs of gingival enlargement

• Grade I: Enlargement confined to interdental papilla

• Grade II: Enlargement involves papilla and marginal gingiva

• Grade III: Enlargement covers three quarters or more of the

crown

Photographic analysis –Ellis & Seymour

• Criteria for assessing gingival encroachment/overgrowth on adjacent tooth surfaces for a gingival unit (where a discrepancy exists between adjacent teeth, the highest score is awarded).

• 0=no encroachment of interdental papilla onto tooth surface.

• 1=mild encroachment of interdental papilla, producing a blunted appearance to papilla tip.

• 2=moderate encroachment, involving lateral spread of papilla across buccal tooth surface of less than one quarter tooth width.

• 3=marked encroachment of papilla, i.e., more than 1/4 tooth width. Loss of normal papilla form.

Inflammatory Enlargement

Inflammatory Enlargement

Acute Chronic

•More Common… .•Secondary Complication..

Etiology• Prolonged exposure to dental plaque………

-Poor oral hygiene-Malocclusion-Hypofunction-Cervical cavities

-Overhanging margins-Irritation from clasps & dentures-Nasal Obstructions..-Mouth breathing

Chronic Inflammatory Enlargement

Originates as a slight ballooning of the interdental papilla and/or the marginal gingiva.

Early stages it produces a life preserver-shaped bulge around the involved teeth

Clinical Features

Slow and Painless……….. Acute Infection , Trauma

• Discrete Sessile or Pedunculated mass resembling a tumor

• May undergo spontaneous reduction in size with followed by exacerbation, ulceration

Histopathology Exudative and proliferative features of chronic inflammation

Clinically deep red or bluish red are soft and friable with a smooth, shiny surface, and they bleed easily…Inflammatory cells fluid with vascular engorgement, capillary formation, and associated degenerative changes

Lesions that are relatively firm, resilient, pink……fibroblasts & collagen fibers

Gingival enlargement in Mouth Breathing

•Red and edematous with a diffuse surface shininess of the exposed area

•Maxillary anterior region is the common site of involvement

•Altered gingiva clearly demarcated from the adjacent unexposed normal gingiva

•Exact manner….not known•Harmful affect attributed

surface dehydration

•Klingsberg 1961….Rodent

Acute Inflammatory Enlargement

Gingival Abscess• Localized, Painful, Rapidly expanding lesion ……Sudden onset• Early lesion shows red swelling with smooth shiny surface …

fluctuant….pointed on surface … bursts.• Sometimes adjacent teeth also sensitive

• Etiology – Foreign substance– Toothbrush bristle, – A piece of apple core, – A lobster shell fragment

• Histologically : Purulent Focus surrounded by inflammatory cells.

Drug-induced gingival enlargement

– Anti epileptics: • Phenytoin (Kimball 1939).• Vigabatrin

– Immunosupressants • Cyclosporine.• Tacrolimus

– Dihydropyridines:• Nifedipine, Verapamil, Diltiazem, Nitrendipine,

nicardipine, amlodipine, felodipine, etc.– NSAIDS.– Hormones:

• Oral contraceptive drugs.– Miscellaneous:

• Sodium valproate, erythromycin,etc.

Drugs associated with Gingival Overgrowth

• Drugs modify the inflammatory and immunologic responses of the host to plaque.

• Goldman

3 Classes of drugs

1. Anticonvulsants2. Immunosuppressants3. Calcium channel

blockers

• First reported in 1939 by Kimball associated with chronic usage of the anti-epileptic drug Phenytoin.

• Clinically and histologically, gingival overgrowth induced by different drugs, are virtually indistinguishable.

• Wysocki et al. 1983, Tyldesley & Rotter 1984),

• Prevalence rate differs:– 50% of patients medicated with phenytoin – 30% for cyclosporin – 20% for Nifedipine

• (Angeiopoulous & Goaz 1972, Seymour et al. 1987, Barclay et ai. 1992)

• Children and adolescents >>> Adults• Anterior >>> Posterior gingival tissues.

• Shows…Intra-patient variation, – May reach a "STATE OF EQUILIBRITIM" often within the

first year of commencing medication.• Systemic illness… drug dosage

General features of DIGO

• Starts as a painless, beadlike enlargement of the interdental papilla

• As the condition progresses, the marginal and papillary enlargements unite and results in massive tissue fold covering most part of the crowns.

• When uncomplicated by inflammation, the lesion is mulberry shaped, firm, pale pink, and resilient, with a minutely lobulated surface and no tendency to bleed

• Usually generalized more severe in the maxillary and mandibular anterior regions.

• A genetic predisposition is a suspected factor in determining whether a person treated with phenytoin will develop gingival enlargement or not

• (Hassell T.M. et al)• The enlargement is chronic

and slowly increases in size• When surgically removed, it

recurs • Spontaneous disappearance

occurs within a few months after discontinuation of the drug

Histologic features

• Pronounced hyperplasia of the connective tissue and epithelium

• Acanthosis of the epithelium, and elongated rete pegs extend deep into the connective tissue

• Densely arranged collagen bundles• Increase in the number of

fibroblasts, new blood vessels • Abundance of amorphous ground

substance (Mariani et al)• The enlargement begins as a

hyperplasia of the connective tissue core of the marginal gingiva and increases by its proliferation and expansion beyond the crest of the gingival margin

• In cyclosporine enlargements, the connective tissue appears highly vascular with foci of chronic inflammatory cells, particularly plasma cells

• (Lucas R.M., Howell L.P. et al)

• The “Mature" phenytoin enlargement has a fibroblast to collagen ratio equal to that of normal gingiva from normal individuals.

• Oxytalan fibers are numerous beneath the epithelium and in areas of inflammation (Baratieri A. 1967)

Recurrence

Anticonvulsants

• Merritt and Putnam (1938….

– PHENYTOIN• Effectiveness• Low cost• Availability

Over 60 years

Partial seizure- Phenytoin - Carbamazapine- Phenobarbital

Generalised seizures- Valproic acid

- Phenytoin - Carbamazapine- Phenobarbital

Generalised absence seizures - Ethosuxamide + Valproic acid

• Incidence Rate :– 0% to 84.5% …. Average 50% (Angelopoulos et al.)– Children and institutionalized…..↑ prevalence (Dahllof &

Modeer)

• Progression– One month…– 12-18 months.. Max severity– Decreased rate in the second year.

• Severity– Daily dose – Blood levels– Duration of use

Addy et al (1982) & Kapuar et al. (1973)

Dahllof & Modeer (1986) &Hassell et al. (1991)

• Trough or a minimum threshold level…..

• Usual therapeutic plasma level of phenytoin … 10-20μg

Classification of gingival hyperplasia caused by Dilantin

James R. Babocks( 1974)

Grade-I Minimal: No hyperplasia

Grade-II Moderate: Definite hyperplasia of gingiva, with encroachment on the clinical crown of the teeth, but no interference of function.

Grade-III Severe: Interference with function due to overgrowth of tissue

Rees TD (1993)

Histological Classification [Barak (1987)]

• Grade I – Normal Gingiva - Width of epithelium - 0.3-0.5 mm.

• Grade II – Slight Overgrowth - Width of epithelium 0.5-1.5 mm.

• Grade III- Moderate Overgrowth –Width of epithelium 1.5-3 mm.

• Grade IV – Severe Overgrowth- Width of epithelium 3- 4 mm.

Seymour, Smith and Turnbill 1985

• The degree of gingival thickening on both labial and lingual aspects was graded as follows: – 0 = normal; – 1 = thickening from the normal up to2 mm; – 2 = thickening from the normal greater than

2 mm

• The 2 scores (thickening and gingival encroachment were added, thus giving a hyperplasia score for each gingival unit.

The extent of encroachment of the gingival tissues onto the adjacent crowns was also graded 0, 1, 2 and 3 on the labial and lingual surfaces are also graded

1ST THEORY(Hassell 1981)

• Different subpopulations of fibroblasts • Some of which are capable of high protein and

collagen synthesis • In presence of Phenytoin, the High activity fibroblasts

react and produce a significant increase in collagen production

• Higher concentration than peripheral or systemic circulation

This theory has not been widely accepted

2nd THEORY(Sorrell et al 1971)

• Long-term phenytoin …………….. immunosuppression.– Tissues more susceptible to inflammation

• But other anti-epileptic drugs though they have immunosupressive action don’t cause gingival overgrowth

Hence, this theory also has not been widely accepted

3rd THEORYStaple 1951,1952

• Phenytoin therapy is reported to cause an alteration in the metabolism of adrenal gland secretions

• Supression of ACTH and alteration in pituitary gland activity

• Reduced glucocorticoid synthesis and this has been suggested a an explanation for the gingival overgrowth

Much consideration has been given to this hypothesis

4th THEORYWaxman (1970)

• Patients on phenytoin have low serum level of folic acid

• Drug may reduce the absorption from GIT or block it’s transport across intestinal epithelium

• Also inhibit folate reductase ………• A deficiency results in impaired maturation of

epithelium, rendering C.T. more susceptible to inflammation

• However, it has not been concluded that folic acid supplements reduces or eliminates gingival overgrowth in epileptics taking phenytoin

ImmunosuppressantsCyclosporin

• First isolated in Switzerland… 1970 (Jean Borel)– Used first by Calne et al…. A renal Transplant– Widely used now for prevention of graft rejection

• Primary ..or in com with Steroids

– Various diseases:• IDDM, Behcet’s disease. Rheumatic and psoriatic arthritis,

bullous pemphigoid and pemphigus, Crohn’s diseaseetc– Suppress some humoral immunity ( B lymphocytes) and to a

much greater extent, cell-mediated immunity (T lymphocyes) such as allograft rejection, delayed hypersensitivity.

– Inhibits IL-2 synthesis and release.

– Dosages : 10-20mg/kg BW/day….Serum concentration of 100-400ng/ml

• Adverse effects :– Dose dependent & Frequently reversible

• Gingival overgrowth• Nephrotoxicit & weight gain• Hyperension , Hyperuricaemia, Mild anaemia,

Neurotoxicity …visual disturbances .. Hypertrichosis.• Tacrolimus … adv effects to lesser extent

– (Graffenreid and Krupp;1986)

– Incidence• 25% of renal transplant cases• 38% …cardiac transplants• 37%... Liver transplants

• First cases…of CIGO…Rateitschak-Pluss (1983)– 50 RT cases..developed GE in 4-6 weeks

• 1984 : Tyldesley & Rotter– 36 RT cases

• 1986 : Friskopp & Klintmalm … restricted to keratinised gingiva..but could extend coronally…– Absence in edentulous areas

• More Hyperaemic than PIGO• 1986 : Rostock et al…spontaneous repositioning of

migrated teeth• 1987 : Seymour et al..24 RT patients on Cyclosporin A &

Azathioprine– Significant growth in 3-6 months..– 1988, 1994( Hefti et al.) – 400ng/ml

• Synergistic effects have been reported ….+ calcium channel blockers.

– Slavin and Taylor 1987

Calcium Channel blockers

• Management of cardiovascular conditions ..1978– Hypertension , Angina, : coronary artery spasm, cardiac

arrythemias

– Inhibit Ca ion across the cell membrane of cardiac & smooth muscles

• Dilatation of coronary arteries• Decreased mycardial contractility & oxygen demand

• 1984..first reported case…NIFEDIPINE– Amlodipine, Felodipine, Diltiazem, Nitrendipine and

Verapamil

– Dose dependency… • Rat model (800ng/ml).. Nishikawa et al. 1995• Human studies..not supported…trough or threshold

should precede

• Ellis & Seymour 1993 :– Nifedipine in GCF….. Respondersand Non responders.

• Incidence: 15% - 84%...42.5%

• Not found in edentulous areas…– around implants??..Silverstein et al 1995

Dissimilar drugs …similar effects??

• MOA at the cellular level

– Influence the Ca and Na influx (Mesing 1985, Gelfand 1987).

• This regulates the rate of fibroblast proliferation.

• “The action of various drugs on the Ca and Na influx may provide a unifying hypothesis linking the three dissimilar drugs to a common unwanted effect.”

SEX HORMONES AND ORAL CONTRACEPTIVES

• Most widely used.

• Mostly a combined preparation of estrogen and progesterone.

•Resolves when drug is withdrawn.

•Appears to be a secondary reaction to the presence of local factors.

•Estrogen increases the keratinization of already keratinized tissues.

•Mucosal tissues are thickened

• Tendency to overgrowth and inc activity of epithelial cells.In non-epi tissue, inc in mucopolysaccharide content is observed.

• Progesterone increases the permeability of the gingival vasculature.

• Exacerbate the response, thus optimal plaque control is imperative.

1. Age.2. Genetic predisposition.3. Pharmacokinetic variables.4. Drug induced alterations in Ging C.T.

homeostasis.5. Drug induced action on growth factors.

The Factors Playing A Role In The Pathogenesis Of Digo

Age

• Children and adolescents more susceptible….• Fibroblasts obtained from both Cyclosporin and phenytoin-

induced gingival overgrowth cases failed to show an age-dependent decrease in protein synthesis and collagen production

• Unique fibroblast phenotype • Influence of androgen metabolism.

• "Target" sub-populations of gingival fibroblasts and cause either an increase in collagen synthesis and/or a decrease in collagenase activity.

Genetic predisposition

• Not all Patients manifest Gingival overgrowth• “Responders” and “non-responders”• Gingival fibroblasts exhibit functional Heterogeneity…

– There exists diff subpopulations of fibroblasts

• A genetic predisposition :– Metabolism of the 3 drugs ……Hepatic cytochrome

P450. – Phenytoin – CYP 2C9 – Dihydropyridines & Cyclosporin – CYP3A4

– Cyt P 450 exhibits considerable polymorphism

• Human Lymphocyte Antigen (HLA)

– Relationship between HLA expression and incidence of DIGO (Cebecci 1996a, Margiotta 1996, Pernu 1994, Thomasson 1996).

– HLA-DR1 and HLA-DR2. • HLA-DR1 afforded some degree of protection

against gingival overgrowth• HLA-DR2 may increase the development of this

unwanted effect.

Pharmacokinetic variables

• It’s a “Contentious” issue ….

• Threshold level….. “activate” fibroblasts

• Salivary concentration …both positive and negative correlation– Conflicting results ……… because dental plaque could

act as a reservoir for the drug which is released by the washing effect of the salivary flow.

• GCF– Nifedipine and amlodipine has shown significant

sequestration in GCF in pts with DIGO (Ellis 1992, Seymour 1994).

Concomitant Medication

• Polypharmacy has been studied with phenytoin and cyclosporin Induced GO

• Incidence, Severity and Recurrence rate is higher..(Bokenkamp 1994, Margiotta 1996)

• Prednisolone and Azathioprine generally given in such pts could influence the expression of overgrowth

Drug induced alterations in gingival CT. Homeostasis

• Increase in CT essential feature of all…– Collagen production / Collagen metabolism

• Collagen production controlled by …… co-ordination of transcripted and post transplantation collagen regulatory mechanisms, – Intracellular degradation.

• Controlled by synthesis and release of MMPs and TIMPs

• Histometric analysis– Increase in the ‘normal growth’,

• (ratio remaining unaltered unlike hyperplasia or hypertrophy).

– Increases the level of translatable collagen RNA. – Overproduction of collagen involves increased steady state

level of mRNA and not a decrease in collagen degradation

• Cell culture studies have shown that the – ECM from PIGO fibroblasts facilitates “FIBROBLAST

SPREADING”. ……prostanoid in origin.

• Both Nifedipine and Phenytoin alter the expression of Type I and IV collagen genes.

• CsA induced GO is related to an increase in Type I procollagen mRNA, indicating increased secretion – A membrane receptor or CYCLOPHILIN, a cytosolic

protein which has been identified as a cellular receptor for Cyclosporin

Non-Collagenous Matrix

• Prolonged phenytoin show increased levels of Hexosamine, uronic acid and total protein per wet weight of tissue

• Increased amounts to sulphated glycosaminoglycans ( Hassel 1983)

Alterations in CT. Metabolism

• 1980 Goultch & Shoskan :– PIGO was because of lack of collagen breakdown …

inactive collagenase• 1998 Zebrowski :

– Proved them wrong as the drugs show variable action against all 3 drugs in different patients. • Collagenase activity was increased by nifedipine,

decreased by phenytoin and unaltered by cyclosporin

• 2000 Tipton and Dabbous:– Concluded that the drugs regulate TIMP production

which is probably more significant than a decrease in collagenase activity

Role of Cytokines

• IL-1β, IL-6 may play a role in the fibrogenic responses of the gingiva to these medications

• IL-6 appears to target connective tissue cells such as fibroblasts both by enhancing proliferation and by exerting a positive regulation on collagen and glycosaminoglycan synthesis.

Role of MMP Synthesis & Function

• Human gingival fibroblasts treated with clinically relevant CsA doses exhibit significantly reduced levels of MMP-1 and MMP-3 secretion;

• These reduced levels may contribute to the accumulation of extracellular matrix components

Drug induced action on Growth Factors

• EGF and PDGF have gained significance. .. Modeer 1990

• Phenytoin may cause increase in number of cell surface receptors of EGF, – May cause an alteration of Ging connective tissue

homeostasis, mediated by the action of drug on intra cellular Ca accumulations

• Values for PDGF were significantly higher for phenytoin exposed cells

TGF beta1

• TGF Beta – 1 – most prominent cytokine in mammals. TGF- stimulates ECM deposition, by

• Promoting Matrix synthesis, and• Inhibiting enzymatic degradation of matrix

macromolecules.

• TGF - has been implicated in a variety of diseases like pulmonary fibrosis, renal fibrosis and ore recently Gingival fibromatosis

• Endothelin is amplified by CsA …….. synthesis and activation of TGF - 1.

Other Postulates..• Jyoti Das (2001)

– Dramatic increase in the keratinocyte growth factor (KGF) among the epithelial cells in all types of DIGO thus suggesting the role of KGF in the pathogenesis

• Pernu 2002– Points that the drug starts to accumulate in the

keratinocyte which then increases the mitotic activity .

• Modeer 1992 – Phenytoin results in up regulation of PgE2 which could

cause an increase in GAG synthesis.

Enlargements associated with Systemic Diseases

Mechanisms

1. Magnification of an existing inflammation..• Conditioned Enlargements

2. Manifestation of systemic disease independent of the gingival inflammatory status• Systemic disease causing gingival enlargement• Neoplastic enlargements

Conditioned Enlargements

• Exaggeration or Distortion of gingival response to plaque

• Bacterial Plaque is necessary for initiation….not sole determinant

– 3 types• Hormonal

– Pregnancy– Puberty

• Nutritional– Vitamin c deficiency

Enlargement in Pregnancy• May be marginal and

generalized, Single or multiple tumor-like masses

• Progesterone and Estrogen ……

• These hormonal changes induce changes in vascular permeability leading to gingival edema and an increased inflammatory response to dental plaque

• The subgingival microbiota may also undergo changes, including an increase in Prevotella intermedia

• (Kornmann K.S. 1980)

Marginal enlargement in pregnancy

• Aggravation of previous inflammation• Incidence has been reported as 10% and 70%

• (Barclay S. 1992).

Clinical Picture

• Varies considerably • Generalized and more prominent interproximally than

on the facial and lingual surfaces • Enlarged gingiva is bright red or magenta, soft, and

friable and has a smooth, shiny surface.• Bleeding occurs spontaneously or on slight provocation

Tumor like gingival enlargement

• Not a Neoplasm; it is an inflammatory response to bacterial plaque

• Modified by the patient's condition• Usually appears after the third month of pregnancy • Reported incidence is 1.8% to 5%.

• (Maier AW 1949)

• Lesion appears as a – Discrete – Mushroom like, – Flattened spherical mass – Protrudes from the gingival margin or more

commonly from the interproximal space and is attached by a sessile or pedunculated base

– Generally dusky red or magenta, it has a smooth, glistening surface that often exhibits numerous deep red, pinpoint markings

– Superficial lesion – Consistency varies; the mass is usually semi firm – Usually painless

Histopathology– Central mass of connective tissue, – Newly formed, and engorged capillaries lined by

cuboid endothelial cells – With varying degrees of edema and chronic

inflammatory infiltrate

– Stratified squamous epithelium is thickened, with prominent rete pegs

– Some degree of intracellular and extracellular edema, prominent intercellular bridges, and leukocytic infiltration

Enlargement in Puberty

• Both male and female adolescents

• Appears in areas of plaque accumulation

• Often only the facial gingivae are enlarged with lingual surfaces are relatively unaltered because……mechanical action of tongue

• Similar to chronic inflam…..degree….recurrences.

• After puberty, the enlargement undergoes spontaneous reduction but does not disappear until plaque and calculus are removed

– Sutcliffe P. 1972…Mean no. of sites …time ..max sites …Oral hygiene.. “A pubertal peak in gingival inflammation that was unrelated to oral hygiene factors occurred.”

– Mobelli 1990 …. Capnocytophaga sp. in the initiation of pubertal gingivitis

– Other studies….. Hormonal changes• Increase in the proportion of Prevotella intermedia

and Prevotella nigrescens.

Enlargement in Vitamin C Deficiency

• Classic description of scurvy• Such enlargement is essentially a conditioned response

to bacterial plaque • Acute vitamin C deficiency

– Causes hemorrhage, collagen degeneration, and edema of the gingival connective tissue

• Modify the response of the gingiva to plaque :– Normal defensive delimiting reaction is inhibited, – Extent of the inflammation is exaggerated

– (Glickman 1948).

Possible etiologies..

1. Low levels of vitamin C influence the metabolism of collagen within the gingiva and periodontium affecting tissue to regenerative and repair.

2. Deficiency increases permeability of the oral mucosa to bacterial endotoxin, inulin, dextran…….epithelial barrier function sub-optimum.

3. Optimal levels are needed to maintain integrity of periodontal microvasculature and vascular response to bacterial irritation.

4. Depletion …interfers with microbial ecology…increases pathogenecity.

Clinical features

• Marginal Gingival enlargement • The gingiva is bluish red, soft, and friable and has a

smooth, shiny surface • Hemorrhage occurring spontaneously or on slight provocation

Histologic features

• Surface necrosis with pseudomembrane • Chronic inflammatory cellular infiltration and scattered areas

of hemorrhage, with engorged capillaries• Marked diffuse edema, collagen degeneration, • Scarcity of collagen fibrils or fibroblasts are striking findings

Plasma cell Gingivitis• Atypical gingivitis & Plasma cell gingivostomatitis • Consists of a mild marginal gingival enlargement that

extends to the attached gingiva • Allergic in origin… • Plasma cell granuloma…Localised lesion (Baskar 1988)

Clinical features• Gingiva appears red, friable, and sometimes granular and

bleeds easily• No attachment loss usually…• Located in the oral aspect of the attached gingiva..• An associated cheilitis and glossitis have been reported • Plasma cell gingivitis is thought to be allergic in origin……….

• Spongiosis and infiltration with inflamm cells

• Dense infiltrate of plasma cells in CT… extending upto oral epithelium

Nonspecific Conditioned Enlargement

Pyogenic Granuloma• Tumor-like gingival enlargement that is considered an

exaggerated conditioned response to minor trauma • The exact nature of the systemic conditioning factor has

not been identified

• Clinical Features– Discrete spherical, tumor-like mass with a

pedunculated attachment to a flattened, keloid-like enlargement with a broad base

– It involutes spontaneously to become a fibroepithelial papilloma or persists relatively unchanged for years

– Treatment consists of removal of the lesions plus the elimination of irritating local factors

– The recurrence rate is about 15%.

• Histologic features– Mass of granulation tissue with chronic inflammatory

cellular infiltrate– Endothelial proliferation– Formation of numerous vascular spaces

Inherited Gingival Overgrowth

• Elephantiasis gingivae, • Hereditary gingival hyperplasia,• Idiopathic fibromatosis and• Hypertrophied

• Rare (1 in 750,000) hereditary condition characterized by slow, progressive enlargement of the gingivae.

• Inheritance mode …Autosomal Dominant …

• May occur alone or in conjunction with other abnormalities,

• As part of a syndrome, – Hypertrichosis and epilepsy,

• With or without mental retardation.

Studies have found that gingival fibroblasts cultured from affected individuals generally produce higher levels of TGF-b1, have higher rates of proliferation, and respond to TGF-beta1 by making increased levels of extracellular matrix.

Systemic Diseases Causing Gingival Enlargement

Leukaemia

• Diffuse or marginal, localized or generalized • An oversized extension of the marginal gingiva or Discrete

tumor like inter-proximal mass • Generally bluish red and has a shiny surface • Moderately firm, but there is a tendency toward

friability and hemorrhage • Occurring either spontaneously or on slight irritation

• Associated chronic inflammation• True leukemic enlargement occurs commonly in acute

lukemia but may also be seen in subacute leukemia

Histologic features

– Varying degree of chronic inflammation + mature leukocytes

– Areas of CT infiltrated with immature and proliferating leukocytes

– Engorged capillaries edematous and degenerated CT.

Granulomatous Disease

Wegener's Granulomatosis

• Rare disease characterized by acute granulomatous necrotizing lesions of the respiratory Tact, including nasal and oral defects

• Cause .. Not known…immunologically mediated tissue injury.

• Clinical features– Reddish purple and bleeds easily on stimulation

Sarcoidosis

– Granulomatous disease of unknown etiology – Starts in individuals in their twenties or thirties – Affects predominantly blacks and can involve almost any

organ– In gingiva - red, smooth, painless enlargement may appear

– Discrete , noncaseating whorls of epithelioid cells and multinucleated giant cells.

Neoplastic enlargement• Gingival Tumors

– Benign• Fibroma • Papilloma • Peripheral Giant Cell Granuloma • Central Giant Cell Granuloma • Other

– Nevus– Myoblastoma– Hemangioma – Neurilemoma– Neurofibroma – Mucoceles– Ameloblastoma

• Malignant Tumors of the Gingiva– Carcinoma

• Squamous cell carcinoma • Malignant Melanoma

– Sarcoma• Fibrosarcoma• Lymphosarcoma• Reticulum cell sarcoma• Kaposi’s sarcoma

False Enlargements

• Not true enlargements of the gingival tissues – Appear as such as a result of increases in size of the

underlying osseous or dental tissues. – The gingiva usually presents with no abnormal clinical

features except the massive increase in size of the area.

• Underlying Osseous Lesions– Examples - Tori and exostoses, Paget's disease, Fibrous

dysplasia, Cherubism, Ameloblastoma

• Underlying Dental Tissues – Examples - Developmental enlargements seen in

primary dentition

TREATMENT

Treatment of gingival enlargement based on understanding of the cause and underlying pathology

changes.

Chronic Inflammatory enlargement • Scaling and root planing

Fibrotic component that does not undergoes shrinkage after scaling and root planing

Surgical removal is the treatment of choice.

•Two techniques available -–Gingivectomy –Flap operation

Soft and friable even after SRP gingivectomy is the treatment of choice.

If all attached gingiva creating mucogingival problem flap operation is indicated

Abscesses

Acute Periodontal Abscess

• Patients general systemic response should be evaluated

• Rise in temperature fever and feeling of malaise should be noted and proper antibiotic regime started

• Drainage established through the pocket or through external incision

Gingival Abscess

• Drainage• Warm saline gargles

• If residual size too great… remove surgically.

Treatment of chronic periodontal abscess

• Adequate drainage, antibiotic treatment

Drug associated gingival enlargement

• First, consideration should be given to the possibility of discontinuing the drug or changing the medication – Substitution with suitable alternative

– 1 to 8 weeks for resolution of gingival lesions.– Unfortunately, not all patients respond to this mode of

treatment, especially those with longstanding gingival lesions.

• Phenytoin: lomatrigine, gabapentin, sulthiame, and topiramate

• Nifedipine: vasodilators, isradipine,• CsA : Tacrolimus (FK506)

• Second, the clinical should emphasize plaque control as the first step in the treatment of drug induce enlargement

• Third, if gingival enlargement persists after consideration of the above mentioned approaches, the cases need to be treated by surgery i.e., gingivectomy or periodontal flap.

3 modes of surgical approach

• Conventional technique– Gingivectomy Knives– Scalpel

• Electrosurgery

• Lasers

Treatment of leukemic gingival enlargement

• Mostly with Acute / Subacute cases… rarely with chronic

• Consultation with patient’s Physician and Hematologist• Superficial Scaling in localized area under topical

anaesthesia… management of bleeding• Progressive deeper scaling is done in subsequent visits.• Systemic antibiotic coverage

Treatment of gingival enlargement in pregnancy

• Elimination of all local irritants.

• Marginal and interdental inflammation are treated by scaling and curettage

• Treatment of tumor like gingival enlargement consists of surgical excision and SRP.

• Lesion should be removed surgical during pregnancy only if they interfere with mastication or produce aesthetic disfigurement that the patient wishes removed.

Recurrence of gingival enlargement

• Most common problem in the management of gingival enlargement. – Residual local irritation, systemic or hereditary or

causative factors for recurrence

• Recurrence during healing period is manifested as red bead like granulomatus masses that bleed on slight provocation

• Condition is corrected by removing the granulation tissue and SRP.

• Familial or hereditary gingival enlargement recurs even if all local factors have been removed.

Summary & Conclusion

Hi Doc, Remember me ?? ……

References

• Textbook of Clinical Periodontology- Fermin A. Carranza: 8th-9th edition

• Textbook of Clinical Periodontology and Implantology - Jan.Lindhe 4th edition

• Contemporary Periodontics - Genco, Goldman, Cohen.• Informational Paper – Drug -Associated Gingival enlargement

JP 2004• Connective tissue metabolism and Gingival overgrowth :

Trackman 2004• Risk factors associated with Gingival overgrowth-JCP 2000• The role of drugs in pathogenesis of gingival overgrowth ; A

collective review of current concepts: Perio 2000 1999• A clinical review of drug-induced overgrowths : Bartold M 1999• Pathogenesis of Drug Induced Gingival Overgrowth- JCP 1996.