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Gngival enlargement
 

Gngival enlargement

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    Gngival enlargement Gngival enlargement Presentation Transcript

    •  
    • DEFINITION
      • Increase in the size of the gingiva is termed as gingival enlargement or gingival overgrowth.
    • 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
      • 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
    • 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
    • B). Generalized involving the gingiva throughout the mouth.
      • C). MARGINAL : Confined to the marginal gingiva.
      • D). Papillary : Confined to the interdental papilla
      • E). Discrete : An isolated sessile or pendunculated tumor like enlargement
      • F). Diffuse ; Involving the marginal and attached gingivae and papillae
      • 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
      • Grade 0 Grade I
      • Grade II Grade III
    • INFLAMATORY ENLARGEMENT
      • Gingival enlargement may result from chronic or acute changes.
      • Chronic inflammatory enlargement Etiology :
      • Prolonged exposure to dental plaque
      • poor oral hygiene
      • irritation by anatomic abnormalities
      • improper restorative & orthodontic appliances.
      • Mouth breathing habit
      • Clinical features :
      • Site - interdental, marginal, attached gingiva
      • may be localized or generalised.
      • Shape - slight ballooning to life preserver shaped bulge
      • slow progressing and painless
      • painful ulceration sometimes
      • Chronic inflammatory enlargement in a 27 year old woman
      • Chronic inflammation associated with mouth breathing in a 16 year old child
      • Histology :
      • chronic inflammatory cells (Lymphocytes, macrophages, plasma cells etc.)
      • lesions deep red, soft, friable, smooth
      • bleeds easily due to vascular engorgement
      • abundant fibroblasts & collagen fibers
      • Acute inflammatory enlargement
      • Gingival abscess
      • Etiology:
      • Bacteria carried deep into the tissues by toothbrush bristles, piece of apple coat etc.
      • Clinical features:
      • site - marginal and interdental gingiva
      • localized, painful, rapidly expanding.
      • Within 24 to 28 hrs lesion becomes fluctuant & purulent exudate expressed as surface orifice & rupture spontaneously.
      • Gingival enlargement in the case of acute necrotising gingivitis
      • Gingival abscess
      • Histopathology:
      • epithelium - varying degree of intra& extracellular oedema.
      • Leukocytic invasion & ulceration
      • connective tissue- purulent focus surrounded by PMNs.
      • edematous tissue
      • vascular engorgement.
      • Periodontal abscess :
      • involves the supporting periodontal tissues.
      • DRUG INDUCED GINGIVAL ENLARGEMENT .
      • Anticonvulsants
      • Immunosuppressants
      • Calcium channel blockers
      • affects th speech, mastication, tooth eruption, and aesthetics problems
      • General clinical features:
      • site - interdental papilla, facial and lingual gingival margins
      • Starts as a bead massive tissue fold covering the crown
      • 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
      • secondary inflammation
      • red, bluish colored lobulated demarcations, increased bleeding
      • Regress spontaneously within few months after discontinuation of the drug.
      • Histopathology :
      • Epithelium - acanthosis, elongated rete pegs
      • conn. Tissue - densely arranged collagen bundles, fibroblasts, neovascularisation
      • abundance of amorphous ground substance
      • cyclosporins - Highly vascularised & foci of chronic inflammatory cells
      • phenytoin - fibroblast to collagen ratio normal, oxytalan fibers are numerous
      • 1).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
      • in systemic administration accelerates the healing of gingival wounds in non- epileptic humans.
      • Mechanism: PHENYTOIN
      • stimulates fibroblast production of an
      • proliferation inactive fibroblastic
      • collagenase
      • gingival overgrowth
      • increase in the sulfated decrease in the
      • glycosaminoglycans in collagen degradation
      • vitro.
      • Phenytoin gingival enlargement on the facial surface
      • Phenytoin gingival
      • enlargement on the
      • occlusal surface
      • Phenytoin enlargement in the posterior region
      • Phenytoin gingival
      • enlargement -
      • close-up view of
      • anteriors.
      • 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.
      • Cyclosporine induced gingival enlargement
      • in a 14yr old boy
      • 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
      • Nifedipine induced gingival enlargement
      • 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 appearance
      • Severe cases jaw appears distorted due to bulbous enlargement
      • secondary inflammation
      • Histopathology:
      • epithelium -thickened & acanthosis elongated rete pegs.
      • Conn. Tissue- highly vascular, densely arranged collagen bundles & numerous fibroblasts
      • 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
      • 2). Manifestation of systemic disease independent of the inflammatory status of the gingiva.This group 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
      • 3 types
      • a) Enlargement in pregnancy
      • b) Enlargement in puberty
      • c) Enlargement in vitamin C deficiency
    • 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.
    • 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
      • - 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.
    • 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
    • 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
      • Gingival englargement with ulceration due to severe deficiency of vit C
    • 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
      • Histopathology:
      • -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
      • -pedunclated, keloid like
      • -red friable with ulceration
      • -fibroepithelial papilloma
      • 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
    • 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
      • Leukaemic gingival enlargement
      • Histopathology:
      • Epithelium - varying degree of leukocytic infiltration & edema
      • Psuedomembranous meshwork of fibrins, necrotic epithelial cells, PMNS & bacteria.
      • Conn.. Tissue - infiltrated with a dense mass of immature & proliferating leukocytes
      • engorged capillaries
    • 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 :
      • reddish purple bleeds easily
      • Histopathology:
      • chronic inflammatory giant cells & foci of acute inflammation, microabscesses
      • Red hemorrhagic mass surrounding gingiva
    • Sarcoidiosis
      • Etiology unknown
      • red, smooth, painless enlargement
      • histopathology discrete, noncaseating whorls of epitheloid cells & multinucleated
      • foreign-body-type giant cells
    • 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.
      • Histopathology:
      • Bundles of well formed collagen fibers.
      • Multinucleated fibroblasts in Giant cell fibroma
    •  
      • 2). Papilloma :
      • proliferation of surface epithelium associated with human papilloma virus(HPV)
      • cauliflower like protuberances
      • broad, hard
      • Human Pappilloma Virus(HPV)
      • histopathology:
      • Finger like projections of stratified squamous epithelium, often hyperkeratotic
      • fibrovascular core
    • 3)Peripheral giant cell granuloma
      • Clinical features
      • interdentally, gingival margin
      • pedunclated, smooth, multilobulated, ulcerations
      • painless, firm , spongy
      • locally invasive destroys underlying bone
      • Histopathology :
      • Numerous foci of multinucleated giant cells & hemosiderin particles
      • chronic infiltration
      • Peripheral giant cell granuloma
      • Hyperplastic epithelium
      • 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
      • Histopathology
      • hyperkeratosis acanthosis
      • premalignant cahnges with atypical epithelium
      • dysplastic changes
      • carcinoma in situ
      • inflammatory infiltration
    • Gingival cyst
      • Localized, marginal& attached
      • mandibular canine & premolar areas
      • painless& erodes the bone
      • Cyst developers from odontogenic epithelium
      • Histopathology
      • flattened, localized thickening of epithelium
      • Other benign tumors- Nevus, Myoblastoma, hemangioma, neurilemmoma, neurofibroma, ameloblastoma
    • 2).Malignant tumors
      • Carcinomas
      • 3% of all malignant tumors in the body.
      • squamous cell carcinoma- common
      • clinical features
      • Exophytic, irregular growth, ulcerative, flat, erosive lesions
      • symptomless initially then painful
      • invades the bone
    •  
      • Malignant melanoma
      • site - hard palate& maxillary gingiva
      • localized pigmentation
      • flat or nodular
      • rapid growth with early metastasis
      • arises from melanocytes from the gingiva
      • Sarcoma
      • Fibrosarcoma, lymphosarcoma& reticulum cell sarcoma of gingiva
      • Kaposi’s sarcoma.
    • 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
      • Enlargement called developmental enlargement
      • & persists until junctional epithelium has migrated enamel to CEJ
      • Physiologic
      • complicated by marginal inflammation
    •