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GINGIVAL ENLARGEMENT 1 CLASSIFICATION BASED ON ETIOLOGY INFLAMMATORY ENLARGEMENT Acute Chronic FIBROTIC ENLARGEMENT drug induced enlargement Idiopathic enlargement 2 enlargement associated with systemic disease –Conditioned enlargement Puberty Vita C deficiency Pregnancy Plasma cell gingivitis Nonspecific conditioned enlargement(granuloma pyogenicum) Systemic diseases causing gingival enlargement Leukemia Granulomatous disease(sarcoidosis,wegener’s granulomatosis) 3 Neoplastic enlargement Benign tumors Malignant tumors False enlargement Underlying osseous lesion Underlying dental tissues 4 Criteria for assessing ge Grade I Grade II Grade III Grade IV- 5 CLASSIFICATION BASED ON LOCATION & DISTRIBUTION LOCALISED: limited to the gingiva adjacent to a single tooth or group of teeth Generalized :involving the gingiva throughout the mouth Marginal: confined to the marginal gingiva Papillary: confined to the interdental papilla Diffuse involving the marginal & attached gingiva & papilla Discrete :an isolated sessile or pedunculated tumor like enlargement 6 PREDISPOSING FACTORS AGE-younger age groups are more affected SEX-males are more affected SITE-anterior facial areas especially the canine region is more prone INFLAMMATION-predisposes to enlargement 7 Age AGE-younger age groups are more affected Higher dosage may be administered As age advances the metabolic process in gingival tissue like glycosaminoglycans synthesis reduces 8 Sex SEX-males are more susceptible Progesterone a female sex harmone decreases glycosaminoglycan synthesis by human gingival fibroblasts. 9 SITE Anterior regions are more affected especially the canine region is more prone Buccal side is more affected than lingual. Dentulous areas are more prone than edentulous area Related to plaque control & drying of mucosa . Temperature difference. 10 INFLAMMATION INFLAMMATION-predisposes to enlargement. Enlargement may predisposes to plaque accumulation 11 Drug induced gingival enlargement Calcium channel blockers Immuno suppressants Anti-epileptic 12 Calcium channel blockers Nifedipine Amlodipine Verapamil Dilitiazem Oxodipine 13 Drug discovered-1960 Therapeutic usage-1980 Class I-affect the heart(verapemil) Class II-affect mainly blood vessels &vasodilation(dihydropyridines) Class III-minimal or slight inotropic effects(dilitiazem) 14 M.O.A-alter the Ca++ metabolism ,the influx of Ca++ across the cell membrane is decreased due to reduced membrane permeability. Contraction of muscle cells occurs when increased intracellular Ca++ binds to trophonin & in the presence of ATP causes the myosin bridge to contract the actin filaments. 15 Although dosage & duration of medication were cited as possible explanations no clear evidence available. 16 Histologic features Hyperkeratosis Acanthosis Elongation of rete pegs(test tube shape) Fibroblast with prominent RER 17 Pathogenesis Apoptosis is characterized by nuclear & cytoplasmic condensation,membrane budding,formation of apoptotic bodies, on-random fragmentation of DNA. Calcium plays an important signaling pathway in triggering apoptosis 18 Prolongation of cell life through inhibition of keratinocyte apoptosis. Ca++ is needed for keratinocyte DNA fragmentation. Low Ca++ expresses Bcl-2 gene which suppresses apoptosis High Ca++ expresses Bax gene which induces apoptosis 19 Indirect action of nifedipine may occur by stimulating either production of IL-2 by Tcells or metabolites of testosterone by gingival fibroblasts which in turn stimulates proliferation or increased collagen synthesis. Responsiveness of the cells appear to be inversely proportional to the IL-1 β levels. Medullasin(a neutrophil elastase-like proteases) plays a role in development of inflammation & mechanism is not known. 20 A role of TGFβ,bFGF & heparan sulphate glycosaminoglycan. The site specificity in the accumulation of collagenous proteins in the ECM may be due to the relatively slow synthesis of these proteins in other tissues or because of altered deposition/resorption in susceptible tissues. 21 Immuno suppressants Cyclosporine Tacrolimus 22 cyclosporin Liphophilic cyclic endecapeptide Used in the prevention of organ transplant rejection Peak plasma conc. reached after 3 hrs. Serum half life 17-40hrs. mostly bound to erythrocytes & lipoproteins. only 5% free in plasma. Therapeutic conc-135μg 23 The total amount of drug per weight in tissue can be upto 20-fold greater than in plasma & varies between organs & individuals. 24 Pharmacological action Cs suppresses T-helper cell function leaving T-suppresser cells un affected. Cs selectively suppresses the cellular immune response by interfering with IL-2 production. 25 MOA Drug cyclophilin complex binds & inhibits calcineurin a calcium & calmodulin dependent serine threonine phosphatase. This inactivation prevents dephosphorylation of nuclear factor of activated T-cells(NF-AT) the nuclear import of NF-AT complex & the formation of a transcriptionally active NF-AT complex. the net consequence is inhibition of IL-2. 26 Pathogenesis During plaque induced inflammation the humoral response replaces the cell mediated response. Several cytokines that play important role in humoral response are known to influence connective tissue homeostasis. IL-1β & IL-6 are cytokines known to play regulatory function in periodontal tissue turnover with IL-1β inducing & IL-6 reducing tissue break down. 27 IL-6 is a multifactorial cytokine found to induce final maturation of B-cells into immunoglobulin producing plasma cells. The increase in plasma cell number may promote Cs induced alteration of the cytokine profile within gingival tissue, resulting in disruption of normal connective tissue turn over 28 The immunosuppresed pts had markedly lower no of NK cells which could enhance the ability of Cs to induce proliferative activity not directly, but by disrupting the complex conn tissue-homeostasis mechanism. Cs stimulates TGF-β1,PDGF which promote fibroblast growth & matrix production. Cs reduces the level of MMP-1 & MMP-2 & increases the level of TIMP. 29 Cs reduces gingival prostacyclin(PGI2)synthesis. PGI2 has an antiproliferative effect via increasing cAMP thus gingival overgrowth may result. 30 Perlecan a type of proteoglycans is increased. It has high affinity for growth factors has been attributed to this proteoglycans ,which ia able to retain these factors inside the basement membrane. Perlecan acts as a major reservoir of FGF-2. 31 Cs could mimic endogenous signals for wound repair or remodelling,but at the usual therapeutic dosage levels& in the absence of any specific inflammatory process, its effect is sub threshold. However when specific inflammatory processes take place within localized & specific areas the effects of Cs could act synergistically with endogenous signals stimulating excessive repair or growth. 32 Side effects of Cs Hypertension Dihydropyridines are Ca ++ channel blockers used to treat hypertension 33 Rx Conversion to other drugs in the same group-tacrolimus Reduction or withdraval of the drug under medical suoervision if indicated gingivectomy 34 Anti-epileptic Phenytoin Sodium valproate Phenobarbital Vigabatrin 35 Phenytoin Macrophages differ in respect to location, morphology & function & they have been recognized to be major mediator of connective tissue turnover,maintenence & repair. 36 Macrophage 27E10-asociated with production of pro inflammatory cytokinesIL-1,IL-6 & TNF-α A reparative/proliferative Macrophage phenotype RM3/1 associated with production of PDGFβ,TGF- β1,bFGF. Expression of 25F9 antigen is connected with maturation of macrophage & relative decrease in 25F9 indicates that maturation of tissue macrophages have been altered. 37 decreases the level of EGF receptors in gingival fibroblast resulting in increased cellular responsiveness to EGF,which can stimulate cellular DNA synthesis. Phenytoin can stimulate testosterone metabolism & increases the level of 5α-dihydrotestosterone a stimulator of fibroblast growth. 38 Phenytoin interferes with folic acid metabolism & hence causes folic acid deficiency Folic acid is necessary for DNA synthesis, thus tissues with a high turn over could be adversely affected PHT can cause immuno suppresion in long term use like decreased salivary IgA which could favor inflammation. 39 PHT & its metabolite P-HPPA induces the release of factors from monocytes which activate quiescence gingival fibroblast to synthesize DNA. Decreases ACTH which leads to increased somatotrophic harm one which increases fibroblast proliferation. 40 PHT leads to production of collagenase which is inactive. Increased PGE2 leading to increased hyaluronic acid . 41 Rx Conversion to other drugs in the same group Reduction or withdraval of the drug under medical suoervision if indicated gingivectomy 42 Others Erythromycin 43 Acute inflammatory enlargement Gingival abscess Localised,painful expanding lesion that is usually of sudden onset. Generally limited to marginal gingiva or interdental papilla. Red, swelling with a smooth shiny surface. 44 Within 24-48hrs the lesion usually becomes fluctuant & pointed with a surface orifice from which a purulent exudates may be expressed. The adjacent teeth are often sensitive to percussion. 45 Etiology Bacteria carried deep into tissues when a foreign substance such as toothbristle,small traumatic injury. 46 Histopathology Polymorphonuclear leucocytes. Edematous tissue Vascular engorgement 47 Rx Incision and drainage. Abscess.swf 48 Chronic inflammatory enlargement Slight ballooning of the interdental papilla &/or the marginal gingiva. Early stages it produces a life preserver –like bulge around the teeth. Progresses slowly & painless. Enlargement is generally papillary or marginal. 49 Occasionally it may occur as a discrete sessile or pedunculated mass resembling a tumor. Painful ulceration sometimes may occur 50 Prolonged Etiology exposure to dental plaque. Factors that favor plaque accumulation Poor oral hygiene Abnormal relationship of adjacent teeth Overhanging margin Food impaction Orthodontic appliance RPD Nasal obstruction Improperly contoured restoration & 51 Histopathology Exudative & proliferative features of chronic inflammation is seen. Edematous tissue Inflammatory cells Vascular engorgement Fibrotic tissue Abuntance of fibroblasts & collagen fibers 52 Treatment Removal of plaque Control of inflammation Scaling & root planning Fibrotic enlargement –gingivectomy. 53 Enlargement associated with mouth breathing Gingiva appears red & edematous Diffuse surface shininess of the exposed area Common site-maxillary anterior region. Attributed to irritation from surface dehydration 54 Idiopathic gingival enlargement Gingivostomatosis Elephantiasis Diffuse fibroma Familial elephantiasis Idiopathic fibromatosis Hereditary gingival hyperplasia Congenital familial fibromatosis 55 Clinical features It affects the attached gingiva as well as the marginal gingiva & interdental gingiva. Pink, firm & almost leathery in consistency & has a characteristic minutely pebbled surface. In severe cases the teeth are almost covered & projects into the vestibule. Jaws appears distorted because of bulbous enlargement. 56 Combined enlargement Gingival hyperplasia is complicated by secondary inflammatory changes because it produces conditions favorable for accumulation of plaque by accentuating the depth of gingival sulcus. It consist of 2 portions. A primary or basic hyperplasia of the connective tissue & epithelium. A secondary complicating inflammatory component 57 Enlargement associated with systemic disease Conditioned enlargement The condition itself does not cause the condition, the altered tissue metabolism accentuates the response to local irritants. Magnification of an existing inflammation initiated by dental plaque. Puberty Pregnancy(harmonal) Vita C deficiency (nutritional disturbances) 58 Enlargement in pregnancy Pregnancy does not cause the condition, the altered tissue metabolism in pregnancy accentuates the response to local irritants. Gingival enlargement in pregnancy is called ANGIOGRANULOMA. Enlargement may be marginal, mostly generalized & more prominent in interdental papilla. Sometimes it occur as a discrete, mushroom like flattened spherical mass attached by a sessile pedunculated base. 59 Puberty 60 Vita C 61 Non specific conditioned enlargement Granuloma pyogenicum – is a tumour like enlargement that is considered an exaggerated response to minor trauma. 62 Systemic diseases causing gingival enlargement Leukemia Granulomatous disease Sarcoidosis wegener’s granulomatosis 63 Neoplastic enlargement Benign tumors Epulis – is a generic term used clinically to designate all discrete tumors & tumor like masses of the gingiva. Most epulis are inflammatory rather than neolastic. 64 Benign tumors Fibroma Papilloma Peripheral giant cell granuloma Central giant cell carcinoma Gingival cyst Leukoplakia 65 Malignant tumors Squamous cell carcinoma Malignant melanoma Metastasis – – – – – – – Adenocarcinoma of colon Lung carcinoma Primary hepatocellular carcinoma Renal cell carcinoma Hypernephroma Chondrosarcoma Testicular tumor 66 67 68 Apoptosis 69 Rx gingivectomy Scaling.swf gingivoplasty.swf 70