GOOD MORNING

GINGIVAL ENLARGEMEN

T

CONTENTS

DEFINITION

CLASSIFICATIONS

CLINICAL-FEATURES,ETIOLOGY, HISTOPATHOLOGY AND TREATMENT

SYNDROMES ASSOCIATED

CONCLUSION

REFERENCES

DEFINITIONIncrease in size of

gingiva or gingival

overgrowth.

Carranza 11th edition.

GINGIVAL ENLARGEMENT CAN BE CLASSIFIED ACCORDING TO ETIOLOGIC FACTORS AND PATHOLOGIC CHANGES AS FOLLOWS I. Inflammatory enlargement A.Chronic B.AcuteII.Drug- induced enlargement.III.Enlargement associated with systemic diseases or conditions A.Conditioned enlargement. 1.Pregnancy 2.Puberty 3.Vitamin C deficiency 4.Plasma cell gingivitis. 5.Nonspecific conditioned enlargement(pyogenic granuloma) B.Systemic diseases causing gingival enlargement 1.Leukemia. 2.Granulomatous diseases(e.g.,Wegener’s granulomatosis,sarcoidosis)IV. Neoplastic enlargement(gingival tumors) A.Benign tumors B.Malignant tumorsV. False enlargement.

ON THE BASIS OF LOCATION AND DISTRIBUTION

LOCALIZED GENERALISED MARGINAL

PAPILLARY DIFFUSE

DISCRETE

THE DEGREE OF GINGIVAL ENLARGEMENT CAN BE SCORED AS FOLLOWS

Grade 0

Grade I

Grade II

Grade III

CHRONIC INFLAMMATORY ENLARGEMENTCLINICAL FEATURES Site - interdental papilla and marginal gingiva. Shape -Life preserver shaped bulge can

increase in size until it covers part of crowns.

May be localized or generalized.

Progresses slowly and painlessly.

Painful ulceration sometimes.

CHRONIC INFLAMMATORY

HISTOPATHOLOGY• Exudative and proliferative features.

• Lesions that are clinically deep red or bluish redsoft and friable,bleed easily due to vascular engorgement.

• Lesions that are relatively firm,resilient and pink hue have a greater fibrotic component with an abundance of fibroblasts and collagen fibres.

TREATMENTScaling and Curettage.

Surgical removal

Gingivectomy and Flap operation.

Enlargment with significant fibrotic

component

If the size of enlargemrnt interferes to root surface

deposits

ETIOLOGY• Prolonged exposure to dental plaque • poor oral hygiene • irritation by anatomic abnormalities • improper restorative & orthodontic appliances. • Mouth breathing habit .

ACUTE INFLAMMATORY ENLARGEMENT GINGIVAL ABSCESS ETIOLOGYBacteria carried deep into the tissues when a foreign substance like toothbrush bristles, piece of apple core

etc.is forcefully embedded into gingivaCLINICAL FEATURES: • site - marginal gingiva or interdental papilla

• localized, painful, rapidly expanding.

• Within 24 to 48 hrs lesion becomes fluctuant & pointed with a surface orifice from which a purulent exudate may be expressed.

GINGIVAL ABSCESS

HISTOPATHOLOGY Surfaceepithelium • Varying degree of intra and extracellular oedema. • Leukocytic invasion & ulceration

Connective tissue• purulent focus surrounded by PMNs. • edematous tissue • vascular engorgement.

PERIODONTAL ABSCESS • involves the supporting periodontal tissues.

TREATMENTCause of the abscess should be removed.

Drainage can be established .

If lesion persists it can be curetted under L.A. or incised.

If persistent and severe systemic antibiotic may be prescribed.

Any residual pockets subgingival curettage or localized gingivectomy.

DRUG INDUCED GINGIVAL ENLARGEMENT Anticonvulsants Immunosuppressants Calcium channel blockers • affects the speech, mastication, tooth eruption,

and aesthetics problems.

General clinical features: • site - interdental papilla, facial and lingual

gingival margins

• Starts as a painless beadlike enlargement of the interdental papilla

• mulberry shaped , firm , pale pink, resilient • no tendency to bleed• appears to project from beneath the gingival

margin separated by a linear groove . • Plaque control becomes difficult resulting in secondary inflammation. produce

• red, bluish discoloration, obliterate lobulated surface demarcations and increase bleeding tendency.

• Regress spontaneously within few months after discontinuation of the drug.

HISTOPATHOLOGY • Epithelium - acanthosis, elongated rete pegs .• Connective Tissue - densely arranged collagen

bundles, fibroblasts, neovascularisation • abundance of amorphous ground substance .

• CYCLOSPORINE- Highly vascularised & foci of chronic inflammatory cells.

• PHENYTOIN - fibroblast to collagen ratio

normal, oxytalan fibers are numerous .

ANTICONVULSANTS • First gingival enlargement reported .• Introduced by Merritt and Putnam in 1938. • Drugs used for the treatment of epilepsy. • Phenytoin, ethotoin, mephenytoin, succinimides

etc. • 50% of the patients • younger patients more prone .• appears in saliva • systemic administration accelerates the

healing of gingival wounds in non- epileptic humans.

• MECHANISM(PHENYTOIN )

Fibroblasts from a phenytoin induced gingivalovergrowth show increased synthesis of sulfated

glycosaminoglycans in vitro

Phenytoin may induce a decrease in collagen-degradation as a result of the production of an

inactive fibroblastic collagenase.

PHENYTOIN INDUCED

IMMUNOSUPPRESSANTS • CYCLOSPORINES used to prevent organ

transplant rejection & to treat autoimmune origin diseases.

• if dosage > 500mg/day reported to induce gingival enlargement.

• 30% patient. • More vascularised .• associated with nephrotoxicity, hypersensitivity,

hypertension, hyperthricosis.

CYCLOSPORINE INDUCED

CALCIUM CHANNEL BLOCKERS (nifedipine,diltiazem, felodipine, nitrendipine and

verapamil)• used for CVS disorders, hypertension , angina

pectoris, coronary artery spasm & cardiac arrhythmia.

• Nifedipine induces enlargement in 20% cases

• Nifedipine + cyclosporines (for kidney transplant)

• larger overgrowth • dose dependent growth

NIFEDIPINE INDUCED

IDIOPATHIC GINGIVAL ENLARGEMENT • termed as gingivostomatitis, elephantiasis,

idiopathicfibromatosis, hereditary gingival hyperplasia & congenital familial fibromatosis.

ETIOLOGY : • unknown • hereditary basis (autosomal dominant or

recessive) • begins with primary & secondary dentition

eruption.

CLINICAL FEATURES: • Site - attached gingiva, gingival margin, and

interdental papilla • pink,firm and leathery with pebbled surface.

• Teeth are completely covered.

• Severe cases jaw appears distorted due to bulbous enlargement

• secondary inflammation

HISTOPATHOLOGY: • Epithelium -thickened & acanthotic with

elongated rete pegs. • Connective Tissue- relatively avascular,

densely arranged collagen bundles & numerous fibroblasts

ENLARGEMENT ASSOCIATED WITH SYSTEMIC DISEASES

• Many systemic diseases oral manifestations two different mechanisms

1. Magnification of existing inflammation

initiated by dental plaque.. “Conditioned enlargement”

2. Manifestation of the systemic disease independent of the inflammatory status of the gingiva.This group is described as “ Systemic diseases causing gingival enlargement”.

CONDITIONED ENLARGEMENT

• systematic condition of the patient exaggerates the usual gingival response to dental plaque.

• bacterial plaque is necessary for its initiation. a). Hormonal conditions (pregnancy &

puberty) b). Nutritional (vitamin C deficiency) c). Non- specific conditioned enlargement

ENLARGEMENT IN PREGNANCY marginal and generalized or single or multiple

tumor like masses.ETIOLOGY - increase in progesterone and

estrogen till 3rd trimester. increased vascular permeability and gingival

edema.

1.MARGINAL ENLARGEMENT results from aggravation of previous

inflammation.

2.TUMOR LIKE GINGIVAL ENLARGEMENT (pregnancy tumor) • inflammatory response to bacterial plaque CLINICAL FEATURES • lesions are discrete, mushroom like, flattened

spherical masses • sessile, pedunculated base• exhibits deep red pin point markings. • Painful ulcerations may occur.

HISTOPATHOLOGY (angiogranuloma) • central mass of connective tissue.• neovascularisation lined by cuboidal

endothelial cells. • varying degree of edema & chronic

inflammatory infiltrate • epithelium thickened, prominent

retepegs.

TREATMENT minimize the potential exaggerated

inflammatory response related to hormonal alteration.

Plaque control,scaling and root planing should be non emergent procedures performed.

Long stressful appointment and periodontal surgical procedures should be postponed until postpartum.

No medications and radiographs Marginal and interdentalScaling and

curettage.Tumor like enlargementSurgical

excisionif possible postpone.

ENLARGEMENT IN PUBERTYCLINICAL FEATURES : • -marginal & interdental (often facial gingiva)• - associated with chronic gingival disease. • -reduces after puberty. • -Capnocytophaga sp.. & P. intermedia

HISTOPATHOLOGY • chronic inflammation with edema.

TREATMENT • Scaling,curretage and oral hygiene

instructions.• Surgical removal may be performed in

severe cases.

ENLARGEMENT IN VITAMIN C DEFICIENCY CLINICAL FEATURES : • Marginal gingivitis • hemorrhage on slight provocation and surface

necrosis with pseudomembrane formation.

HISTOPATHOLOGY(VIT-C)• chronic inflammatory cellular infiltrate with

superficial acute response • scattered areas of hemorrhage • diffuse edema, collagen degeneration &

scarcity of collagen.

PLASMA CELL GINGIVITIS(atypical gingivitis,plasma cell gingivostomatitis )• site- marginal and attached gingiva .

CLINICAL FEATURES : • red, friable, bleeds easily • site-oral aspect of attached gingiva

HISTOPATHOLOGY(Plasma Cell Gingivitis)

• Epithelium- spongiosis and infiltrated with chronic inflammatory cells.

• lower spinous layer and basal layer damaged

• plasma cells infiltrate

NON SPECIFIC CONDITIONED ENLARGEMENT (pyogenic

granuloma)• Tumor like gingival enlargement.• conditioned response to minor trauma.CLINICAL FEATURES: • discrete spherical tumor like mass • red friable with ulceration,purulent exudation. • Involute to become fibroepithelial papilloma.

HISTOPATHOLOGY• chronic inflammation with granulation tissue • vascular spaces & epithelial atrophy

TREATMENT removal of lesion and local irritating factors .

SYSTEMIC DISEASES CAUSING GINGIVAL ENLARGEMENT

LEUKEMIA CLINICAL FEATURES : • diffuse or marginal • localized or generalized tumor like mass in interproximal spaces • red, friable, firm and hemorrhagic • painful necrotising • ulcerative inflammation

HISTOPATHOLOGY • Epithelium - varying degree of leukocytic

infiltration & edema • Psuedomembranous meshwork of fibrins,

necrotic epithelial cells, PMNS & bacteria. • Connective Tissue - infiltrated with a dense

mass of immature & proliferating leukocytes • engorged capillaries.

TREATMENTIn leukemic patients (in general)Refer the patient to physician.Prior to chemotherapy, a complete periodontal

treatment plan should be prepared.Treatment planMonitor hematological lab values dailyAdminister antibiotics prior to any periodontal

therapyExtract non-maintainable or potentially

infectious teeth,atleast 10 days prior to initiation of chemotherapy.

Thorough periodontal debridement is done and oral hygiene instructions are given

During acute phases of leukemia,patients should receive only emergency periodontal care.

• If there is a persistent gingival bleeding• Cleanse the area with 3 percent hydrogen

peroxide.• Carefully explore the area and remove any

etiologic local factors• Recleanse with 3 percent H2O2 place the cotton

pellet soaked in thrombin against bleeding point.

• Cover with a gauze• If oozing persists after removal of gauze,replace

cotton and then place a periodontal dressing over the area for 24 hours.

GRANULOMATOUS DISEASESWEGENER’S GRANULOMATOSIS ETIOLOGY :• cause unknown (immunologically mediated

tissue injury) • characterized by acute granulomatous

necrotising lesion of respiratory tract involving the orofacial region .

CLINICAL FEATURES : • reddish purple bleeds easily.HISTOPATHOLOGY: • chronic inflammatory giant cells & foci of acute

inflammation, microabscesses covered by a thin acanthotic epithelium.

SARCOIDIOSIS ETIOLOGY• unknown. • red, smooth, painless enlargement .

HISTOPATHOLOGY • discrete, noncaseating whorls of

epitheloid cells & multinucleated • foreign-body-type giant cells

NEOPLASTIC ENLARGEMENT (GINGIVAL TUMORS)

Benign tumors of gingiva Malignant tumors

Epulis Squamous cell carcinoma

Fibroma Malignant melanoma

Papilloma Sarcoma Peripheral giant cell granuloma Fibrosarcoma Cental giant cell granuloma Lymphosarcoma Leukoplakia Reticulum cell

carcinoma Gingival Cyst Kaposis sarcoma Other benign masses like nevus Renal cell carcinoma

FALSE ENLARGEMENT• Not true enlargement but appear as an

increase in size of underlying osseous or dental tissues.

• A). Underlying osseous lesions • Enlargement of bone - exostosis or tori (paget’s disease, fibrous dysplasia, cherubism,

central giant cell granuloma, ameloblastoma osteoma, osteosarcoma)

B). Underlying dental tissues • during stages of eruption particularly primary

dentition. • labial gingiva- bulbous marginal distortion called developmental enlargement • & persists until junctional epithelium has

migrated from enamel to CEJ • Physiologic • complicated by marginal inflammation.

CONCLUSION• The treatment of gingival enlargement depends

on the type of clinical enlargement encountered.

• The enlargement can be inflammatory,fibrotic or a combination of both.

• Plaque induced inflammation appears to be a general stimulating effect regardless of the mechanism of gingival enlargement.

• In recent years,flap surgery have been used more often to treat gingival enlargement than gingivectomy.

REFERENCES Clinical periodontology and Implant dentistry(5th

Edition) Jan Lindhe Vol 1.Carranza’s Clinical Periodontology Eleventh

edition.Outline of periodontics,J.D.Manson,B.M.Eley.Essentials Of Periodontology,Sahitya Reddy S.Glickman:Hyperplasia of the gingiva associated

with Dilantin therapy.Hallmon WW,Rossman JA:The role of drugs in the

pathogenesis of gingival overgrowth.Slavin J,Taylor J :Cyclosporine,nifedipine and

gingival hyperplasia .Rushton MA:Hereditary or Idipathic hyperplasia of

the gums

THANK YOUTHANK YOU