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DEFINITION
Increase in the size of the gingiva is termed as gingival enlargement or gingival overgrowth.

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CLASSIFICATION

According to the etiologic factors and pathologic changes. I) Inflammatory enlargement a). Chronic b). Acute II) Drug induced enlargement III) Enlargements associated with systemic diseases A). Conditioned enlargement 1). Pregnancy 2). Puberty

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3). Vitamin C 4). Plasma cell gingivitis 5). Nonspecific conditioned enlargement B). Systemic diseases causing gingival enlargement 1). Leukemia 2). Granulomatous diseases (Wegener’s granulomatosis, sarcodiosis) IV) Neoplastic enlargement A). Benign tumors B). Malignanttumors V) False enlargement
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On the basis of location and distribution

A). Localized:Limited to the gingiva adjacent to a single tooth or group of tooth. eg. The gingival enlargement localized in the canine region

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B). Generalized involving the gingiva throughout the mouth.
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D). Papillary: Confined to the interdental papilla

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E). Discrete: An isolated sessile or pendunculated tumor like enlargement

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F). Diffuse; Involving the marginal and attached gingivae and papillae

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Scoring of gingival enlargement
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

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Grade 0

Grade I

Grade II
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Grade III

INFLAMATORY ENLARGEMENT
Gingival enlargement may result from chronic or acute changes.

Chronic inflammatory enlargement Etiology:
3 Prolonged exposure to dental plaque 3 poor oral hygiene 3 irritation by anatomic abnormalities 3 improper restorative & orthodontic appliances. 3 Mouth breathing habit
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Clinical features : 3 Site - interdental, marginal, attached gingiva 3 may be localized or generalised. 3 Shape - slight ballooning to life preserver shaped bulge 3 slow progressing and painless 3 painful ulceration sometimes

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Chronic inflammatory enlargement in a 27 year old woman
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Chronic inflammation associated with mouth breathing in a 16 year old child

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Histology : 3 chronic inflammatory cells (Lymphocytes, macrophages, plasma cells etc.) 3 lesions deep red, soft, friable, smooth 3 bleeds easily due to vascular engorgement 3 abundant fibroblasts & collagen fibers

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Acute inflammatory enlargement Gingival abscess
Etiology: Bacteria carried deep into the tissues by toothbrush bristles, piece of apple coat etc. Clinical features: 3 site - marginal and interdental gingiva 3 localized, painful, rapidly expanding. 3 Within 24 to 28 hrs lesion becomes fluctuant & purulent exudate expressed as surface orifice & rupture spontaneously.

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Gingival enlargement in the case of acute necrotising gingivitis
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Gingival abscess
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Histopathology: 3 epithelium - varying degree of intra& extracellular oedema. Leukocytic invasion & ulceration 3 connective tissue- purulent focus surrounded by PMNs. 3 edematous tissue 3 vascular engorgement.

Periodontal abscess:
involves the supporting periodontal tissues.
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DRUG INDUCED GINGIVAL ENLARGEMENT.
„ Anticonvulsants „ Immunosuppressants „ Calcium channel blockers affects th speech, mastication, tooth eruption, and aesthetics problems General clinical features: 3site - interdental papilla, facial and lingual gingival margins

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massive tissue fold covering 3 Starts as a bead the crown 3 mulberry shaped , firm , pale pink, resilient 3 no tendency to bleed 3 appears to project from beneath the gingival margin separated by a linear groove. 3 Plaque control becomes difficult secondary inflammation red, bluish colored lobulated demarcations, increased bleeding

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3 Regress spontaneously within few months after discontinuation of the drug. Histopathology: 3 Epithelium - acanthosis, elongated rete pegs 3 conn. Tissue - densely arranged collagen bundles, fibroblasts, neovascularisation 3 abundance of amorphous ground substance 3 cyclosporins - Highly vascularised & foci of chronic inflammatory cells 3 phenytoin - fibroblast to collagen ratio normal, oxytalan fibers are numerous
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1).Anticonvulsants
© First gingival enlargement reported © Introduced by Merritt and Putnam in 1938. 2 Drugs used for the treatment of epilepsy 2 Phenytoin, ethotoin, mephenytoin, succinimides etc. 2 50% of the patients 2 younger patients more prone 2 appears in saliva 2 in systemic administration accelerates the healing of gingival wounds in non- epileptic humans.
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Mechanism:

PHENYTOIN production of an inactive fibroblastic collagenase

stimulates fibroblast proliferation gingival overgrowth

increase in the sulfated decrease in the glycosaminoglycans in collagen degradation vitro.
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on the

Phenytoin gingival enlargement facial surface

Phenytoin gingival enlargement on the occlusal surface
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Phenytoin enlargement in the posterior region

Phenytoin gingival enlargement close-up view of anteriors.
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2). Immunosuppressants
© Cyclosporines used to prevent organ transplant rejection & to treat autoimmune origin © if dosage > 500mg/day reported to induce gingival enlargement. © 30% patient. © More vascularised © associated with nephrotoxicity, hypersensitivity, hypertension, hyperthricosis.
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enlargement

Cyclosporine induced gingival in a 14yr old boy

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3).Calcium channel blockers
© used for CVS disorders, hypertension, angina pectoris, coronary artery spasm & cardiac arrhythmia. © Drugs like nifedipine,diltiazem, felodipine, nitrendipine and verapamil. © Nifidipine induces enlargement in 20% cases © Nifidepine + cyclosporines (for kidney transplant) larger overgrowth © dose dependent growth
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Nifedipine induced gingival enlargement

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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.
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Clinical features:  Site - attached gingiva, gingival margin, and interdental papilla  pink,firm and leathery with pebbled appearance  Severe cases jaw appears distorted due to bulbous enlargement  secondary inflammation
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Histopathology:  epithelium -thickened & acanthosis elongated rete pegs.  Conn. Tissue- highly vascular, densely arranged collagen bundles & numerous fibroblasts

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ENLARGEMENT ASSOCIATED WITH SYSTEMIC DISEASES
Many systemic diseases can develop oral manifestations that mayaffect the periodontium by two different mechanisms 1). Magnification of existing inflammation initiated by dental plaque “Conditioned enlargement” a). Hormonal conditions(pregnancy & puberty) b). Nutritional (vitamin C deficiency) c). Non- specific conditioned enlargement
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2). Manifestation of systemic disease independent of the inflammatory status of the gingiva.This group described as “Systemic diseases causing gingival enlargement”.

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Conditioned enlargement
systematic condition of the patient exaggerates the usual gingival response to dental plaque bacterial plaque is necessary for its initiation 3 types a) Enlargement in pregnancy b) Enlargement in puberty c) Enlargement in vitamin C deficiency
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A) Enlargement in pregnancy
Marginal and generalized

Etiology- increase in progesterone and estrogen till 3rd trimester - increased vascular permeability and gingival edema. Marginal enlargement Clinical features -generalized and interproximal - bright red, soft friable and bleeds spontaneously.

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Tumor like gingival enlargement
Also called pregnancy tumor inflammatory response to bacterial plaque clinical features -lesions are discrete, mushroom like, flattened spherical masses -sessile, pedunclated -exibits deep red pin point margins. -Painful ulcerations

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-

histopathology: called angiogranuloma. central mass of connective tissue neovascularisation lined by cuboidal endothelial cells. -varying degree of edema & chronic inflammatory infiltrate - epithelium thickened, prominent retepegs. Preventable by removal of plaque & calculus.

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B) Enlargement in Puberty
In both male & female adolescents Clinical features : -marginal & interdental -chronic gingival disease -reduces after puberty -Capnocytophaga sp.. & P. intermedia Histopathology -chronic inflammation with edema

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C) enlargement in Vitamin C deficiency
Clinical features : - Marginal gingivitis - hemorrhage on slight provocation and suface necrosis with pseudomembrane formation Histopathology: - chronic inflammatory cellular infiltrate with superficial acute response - scattered hemorrhage - diffuse edema, collagen degeneration & scarcity of collagen

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Gingival englargement with ulceration due to severe deficiency of vit C
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Plasma cell gingivitis
Referred to as atypical gingivitis and plasma cell gingivostomatitis site- marginal and attached gingiva Clinical features : -red, friable, bleeds easily -oral aspect of attached gingiva

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Histopathology: -epithelium- spongiosis and infiltrated with chronic inflammatory cells. -lower spinous layer and basal layer damaged -plasma cells infiltrate

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Non specific conditioned enlargement (pyogenic granuloma)
Tumor like gingival enlargement conditioned response to minor trauma Clinical features: -discrete spherical tumor like mass -pedunclated, keloid like -red friable with ulceration -fibroepithelial papilloma

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Histopathology: -chronic inflammation with granulation tissue -vascular spaces & epithelial atrophy Treatment - removal of lesion and local irritating factors

gingival mass at the

mass regress 3

time of pregnancy

months after pregnancy

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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
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Leukaemic gingival enlargement
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Histopathology: 3 Epithelium - varying degree of leukocytic infiltration & edema 3 Psuedomembranous meshwork of fibrins, necrotic epithelial cells, PMNS & bacteria. 3 Conn.. Tissue - infiltrated with a dense mass of immature & proliferating leukocytes 3 engorged capillaries

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Granulomatous diseases
Wegener’s granulomatosis
Etiology: cause unknown (immunologically mediated tissue injury) Characterized by acute granulomatous necrotising lesion of respiratory tract involving the orofacial region Clinical features: 3 reddish purple bleeds easily Histopathology: 3 chronic inflammatory giant cells & foci of acute inflammation, microabscesses
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Red hemorrhagic mass surrounding gingiva
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Sarcoidiosis
Etiology unknown red, smooth, painless enlargement histopathology discrete, noncaseating whorls of epitheloid cells & multinucleated foreign-body-type giant cells

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NEOPLASTIC ENLARGEMENT (GINGIVAL TUMORS)
A).Benign tumors of gingiva Epulis all discrete tumors & tumor like masses of gingiva considered inflammatory growth of gingiva & hard palate 1)Fibroma - arises from connective tissue or
PDL slow growing, firm, nodular, soft, vascular, pedunculated.

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Histopathology: Bundles of well formed collagen fibers. Multinucleated fibroblasts in Giant cell fibroma

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2). Papilloma:
3 proliferation of surface epithelium associated with human papilloma virus(HPV) 3 cauliflower like protuberances 3 broad, hard
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Human Pappilloma Virus(HPV)

histopathology: 3 Finger like projections of stratified squamous epithelium, often hyperkeratotic 3 fibrovascular core
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3)Peripheral giant cell granuloma
Clinical features 3 interdentally, gingival margin 3 pedunclated, smooth, multilobulated, ulcerations 3 painless, firm , spongy 3 locally invasive destroys underlying bone Histopathology: 3 Numerous foci of multinucleated giant cells & hemosiderin particles 3 chronic infiltration
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Peripheral giant cell granuloma

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3 Hyperplastic epithelium 3 ulceration

Central giant cell granuloma
within the jaw and produce central cavitation.

Leukoplakia
Defined as “a white plaque that cannot be diagnosed as any other etiology other than that associated with tobacco chewing”. Etiology- C, albicans, HPV-16, trauma Clinical features - white, flattened, scaly, thick keratinous plaque
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Histopathology 3 hyperkeratosis acanthosis 3 premalignant cahnges with atypical epithelium 3 dysplastic changes 3 carcinoma in situ 3 inflammatory infiltration

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Gingival cyst
3 Localized, marginal& attached 3 mandibular canine & premolar areas 3 painless& erodes the bone 3 Cyst developers from odontogenic epithelium Histopathology 3 flattened, localized thickening of epithelium 3 Other benign tumors- Nevus, Myoblastoma, hemangioma, neurilemmoma, neurofibroma, ameloblastoma
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2).Malignant tumors Carcinomas
3 3% of all malignant tumors in the body. 3 squamous cell carcinoma- common 3 clinical features 3 Exophytic, irregular growth, ulcerative, flat, erosive lesions 3 symptomless initially then painful 3 invades the bone
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Malignant melanoma 3 site - hard palate& maxillary gingiva
3 localized pigmentation 3 flat or nodular 3 rapid growth with early metastasis 3 arises from melanocytes from the gingiva

Sarcoma Fibrosarcoma, lymphosarcoma& reticulum cell sarcoma of gingiva Kaposi’s sarcoma.
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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.

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B). Underlying dental tissues
5 during stages of eruption particularly primary dentition 5 labial gingiva- bulbous marginal distortion 5 Enlargement called developmental enlargement 5 & persists until junctional epithelium has migrated enamel to CEJ 5 Physiologic 5 complicated by marginal inflammation

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