Gingival Enlargement

Contents
Introduction Classification Inflammatory Enlargement Drug induced enlargement. Combined enlargement Enlargements associated with systemic diseases. Conditioned enlargement Systemic diseases causing gingival enlargement Neoplastic enlargement: Malignant Benign. False enlargements Treatment. Conclusion.
2

Introduction
Increase in the size of the gingiva,is called gingival enlargement.

Classification
on the basis of etiologic factor and pathologic changes

Inflammatory enlargements a)Acute b)Chronic Drug induced enlargement Enlargements associated with systemic diseases and condition A. Conditioned enlargement 1.Pregnancy 2.Puberty 3. Vitamin C deficiency

4.Plasma cell gingivitis 5.Nonspecific conditioned enlargement( Granuloma pyogenicum) B. Systemic diseases causing gingival enlargement. Leukemia Granulomatous diseases ( Wegeners granulomatosis, sarcoidosis ) Neoplastic enlargement (gingival tumours) A.Benign tumours B. Malignant tumours False enlargement.
5

On the basis of location and distribution Localised Generalised Marginal Papillary Diffuse Discrete

On the basis of degree of gingival enlargement.

Grade 0 Grade I Grade II Grade III

Inflammatory enlargement.

ACUTE

CHRONIC

Chronic inflammatory enlargement Etiology -Prolonged exposure to dental

plaque
-factors that favour plaque retention

Clinical features
Originate as slight balloning of interdental papilla. Life preserver shape bulge around involved tooth Discrete sessile or pedunclated mass interproximal or on the marginal or attached gingival.

Lesions are usually slow growing and painless.

spontaneous reduction in size followed by exacerbation and continued enlargement.
10

Histopathology Exudative and proliferative features of chronic inflammation. Deep red lesions or bluish red lesions
Soft & friable Smooth and shiny surface Bleed easily Preponderance of inflammtory cells and fluid

firm, resilient and pink lesions

Greater fibrotic component with an abundance of fibroblast and collagen fibers.

11

 In mouth breathers, red and erythematous diffuse surface shininess of exposed area.

Most common site maxillary anteriors. attributed to irritation from surface dehydration. Klingsberg etal (1961) in his study proved that changes in the gingiva could not be produced by air drying the gingiva.

12

treatment
Scaling and root planing If necessary surgical removal:
Gingivectomy Flap operation

13

Acute Inflammatory Enlargement.

Gingival Abscess -Localised, painful, rapidly expanding lesion, usually of sudden onset. -marginal gingival or interdental papilla. -Initially red swelling with a smooth and shiny appearance. 24 to 48 hours, fluctuant and pointed with a surface orifice from which a purulent exudates may be expressed.

-Adjacent teeth are usually sensitive to percussion -If permitted to progress , generally ruptures spontaneously.
14

Etiology
bacteria carried deep into the tissues foreign substance such as a tooth brush bristle , a piece of apple core, or a lobster shell fragment is forcefully embedded in to the gingiva.

15

Histopathology Purulent focus in the connective tissue . diffuse infiltration of polymorphonuclear leukocytes, edematous tissue, vascular engorgement. Surface epithelium intra and extracellular edema, invasion by leukocytes and sometimes ulceration.
16

treatment
Drainage and irrigation of the abscess.

17

Periodontal abscess. -Localised purulent inflammation in the periodontal tissues. -Otherwise called lateral or parietal abscess. Periodontal pocket of 5-8mm Tender on percussion Pain Foul taste Mobility of involved teeth Tenderness over the corresponding gingiva

18

Pathogenesis

Extension of infection from periodontal pocket supporting periodontal tissues. Lateral extension of inflammation from inner surface of a periodontal pocket connective tissue . Formation in a pocket with tortuous course around the root. Incomplete removal of calculus. after trauma to the tooth or in endodontic therapy.

19

Histopathology
viable and nonviable PMNs enzymes. acute inflammatory reaction sorrounding the prulent area epithelium intracellular and extracellular edema and invasion of leukocytes. Localized acute abscess chronic abscess

20

De witt etal (1985) The invading organisms identified were gram negative cocci , diplococci, fusiforms, and spirochaetes. Newmann (1979) microorganisms that colonized the periodontal abscess were primarily gram negative anaerobic rods.

21

treatment
Drainage and irrigation Pocket elimination procedure

22

Drug induced Gingival Enlargement

anticonvulsants immunosuppressants calcium channel blockers create speech, mastication ,tooth eruption, and aesthetic problems. Butler etal (1987) and Seymour etal (1996) reported that the clinical and microscopic features of different drugs are similar.

23

Clinical features.
-a painless beadlike enlargement of the interdental papilla massive fold covering a considerable portion of the crowns may interfere with occlusion. Lesions uncomplicated by inflammation mulberry shaped, firm, pale pink,resilient and minutely lobulated surface and with no tendency to bleed.

24

 usually generalized ,more severe in the maxillary and mandibular anterior regions. areas where teeth are present and absent in edentulous spaces. It dissapears in areas from which teeth are extracted

Malpositioning

25

 chronic and slowly increases in size . When surgically removed It recurs. Spontaneous disappearance few months after discontinuation of the drug. May occur in mouths with little or no plaque and May be absent in mouths with abundant deposits.

26

27

Anticonvulsants
The first drug- induced enlargements were those produced by phenytoin (Dilantin). Introduced by Meritt and Putnam in 1938 All forms of epilepsy except petitmal. Other hydantoins known to induce gingival enlargement are ethotoin (Peganone),Mephenytoin (Mesatoin)

Other anticovulsants that have the same side effect are the succinimides ( ethosuximide zerontin, methosuxinimide celontin,)and valproic acid (Depakene)
28

Seymour etal (1996) Gingival enlargement occurs in about 50% of the patients receiving the drug Different authors have reported incidences from 3% to 84.5%..

29

Pharmacokinetics
Phenytoin
Depresses the motor cortex of CNS Stabilises the neuronal discharge Limits progression of neuronal excitation. Block calcium influx across cell membranes.

30

Pathogenesis
Effect on human gingival fibroblasts Tissue culture experiments by Shafer (1960,1961) phenytoin stimulates proliferation of fibroblast like cells and decrease in degradation of collagen. two analogues of phenytoin(1allyl 5 phenylhydantoinate and 5-methyl-5 phenyl hydantoinate) have similar effect on fibroblast like cells.

31

Effect on donor age.

Babcock(1945) reported that it occurs more often in younger patients.
Johnson et al (1990) Effect of donor age on synthetic properties of fibroblasts. Greater collagen and protein synthesis in young age. Age dependent decrease in synthesis. Vijaya singham et al (1991) failed to detect any fibroblast growth in response to phenytoin invitro.
32

Hassell and Hefti(1991) Phenotypically distinct and different subpopulations of fibroblasts. Phenotoin reacts with some but not all.

33

Increased glycosaminoglycans Dahloff et al (1984) Phenytoin induced enlargementIncreased GAG. Pagiarini et al (1995) Effect of phenytoin induced gingival enlargement on glycosaminoglycan synthesis in fibroblasts. Attached gingival fibroblasts-increased intracellular GAGs Free gingival fibroblasts-extracellular sulfated GAGs Kantor ML et al(1953) reported that fibroblast from a phenytoin induced gingival over growth show increased synthesis of sulfated glycosaminoglycans in vitro.

34

Role of growth factors

Modeer et al (1990) interactive effect with epidermal growth factor. Dill et al (1993) increased production PDGF mediating gingival over growth.

35

Intereference with folic acid absorption amd metabolism

PhenytoinFolic acid deficiency: affects, epithelium, gonads and bone marrow. Brown (1991), Drew (1987) Compramise of oral epitheliuminflammatory alterations of underlying lamina propria in the presence of plaque. Drew (1987) Topical application of folic acid and reduction in gingival overgrowth.

36

Production of inactive collagenase

Hassel (1982) Decrease in collagen degradation Production of inactive fibroblastic collagenase.

Liu(1973),Moy(1985) Decreased activity of collagenase

37

 Seymour (1996) its occurrence are not necessarily related to the dosage after the threshold levels have been exceeded Shapiro (1957) systemic administration of phenytoin accelerates the healing of gingival wounds in nonepileptic humans. increase the tensile strengths of healing in abdominal wound in rats (Decosta1988)

38

Histopathology
Thick stratified squamous epithelium Elongated retepegs extend deep in to the connective tissue. Densely arranged collagen bundles Increase in the number of fibroblasts, New blood vessels. Abundance of amorphous ground substance

39

Combined enlargement
enlargement makes difficult plaque control secondary inflammatory reaction increase in the size red or bluish red discolouration obliterate the lobulated surface demarcations, increased tendency towards bleeding.

40

 Cianco et al(1972),Hall WB(1969),Klar LA(1939)Nuki et al(1972)

inflammation is a perequisite for the development of the enlargement, which therefore could be prevented by plaque control.

However oral hygiene by tooth brushing(Elzay RP1964) or the use of chlorhexidiene toothpaste(Russel 1978) reduces the inflammation but does not lessen or prevent the overgrowth. Dallas B M et al(1963),Dreyer et al (1978) hyperplasia of mucosa in edentulous mouths.

41

Hassell et al (1978) Non-inflamed gingival fibroblasts are less active or even quiescent and do not respond to circulating phenytoin, where as fibroblasts within the inflamed tissue are in an active state as a result of the inflammatory mediators and endogenous growth factors present. Hassell (1994) and Raeste (1978) genetic predisposition is a suspected factor in determining whether a person treated with phenytoin will develop gingival enlargement or not.

42

Immunosupressants
Isolated in Switzerland in 1970 Fungus-Tolypocladium inflatum Gams. Cyclic polypeptide Cyclosporine A (Sandimmune, Neoral) intravenously or by mouth , and dosages greater than 500 mg /day have been reported to induce gingival overgrowth. Immunosupressive action. B cells and to a greater extent T cells. Dosage-10-20mg/kg body weight.

43

Pharmacokinetics.
Specific and reversible inhibition of immunocompetent lymphocytes.(T helper cells) Cyclosporin A inhibits interleukin-2 synthesis. Inhibits the ability of cytotoxic T cells to respond to IL-2. Inhibits the activation of macrophages Prevents the production of IL-1 receptors on the T helper cells.

44

Seymour et al (1987)

Cyclosporine induced gingival enlargement is more vascularised than the phenytoin enlargement. 30% of patients receiving the drug . more frequent in children .
magnitude appears to be related more to plasma concentration than to the patients periodontal status.
45

Thomason et al (1993, 1996) Gingival enlargement is greater in patients who are medicated with both cyclosporine and calcium channel blocking agents.

The microscopic finding of many plasma cells plus the presence of an abundant amorphous extracellular substance has suggested that the enlargement is a hypersensitivity response to the cyclosporine.

46

 Ayanoglou et al (1997 in experimental animals, oral administration of cyclosporine also induced abundant formation of new cementum. Other than gingival enlargement, cyclosporine also induces other major side effects such as nephrotoxicity, hypertension and hyperthricosis Another immunosuppressive drug called tacrolimus has been used effectively and is also nephrotoxic , but it results in much less severe hypertension, hyperthricosis and gingival overgrowth.

47

Clinical manifestations
More pronounced in the labial gingiva. Considerable bleeding on surgical removal. More restricted to keratinised gingiva. May extend coronally Absent in edentulous patients. Soft, red, bluish red, extremely fragile. Caused migration and malposition.

48

Pathogenesis
Cyclosporin A and its metabolite react with phenotypically distinct subpopulations of fibroblastsincrease in protein synthesis, rate of proliferation. Genetic predispositions.HLA -DR1 Iacopino et al(1997) PDGf B and messenger RNA is significantly increased .

49

Histopathology
Connective tissue with an irregular parakeratinised multilayered epithelium.

Epithelial ridges penetrating deep in to the connective tissue.

Connective tissue- highly vascularised

Plasma cells., lesser extent lymphocytes.

Friskopp (1986) T-lymphocytes and monocytes adjacent to the junctional epithelium but no B-lymphocytes. Pisanty et al (1988) More accumulation of noncollagen material and a thickening of epithelium , than increase in the number of fibroblasts.

50

Calcium Channel Blockers Treatment of cardiovascular conditions inhibit calcium ion influx across the cell membrane. Direct dilation of the coronary arteries and arterioles , improving tension by dialating the peripheral vasculature. 15-83% of patients taking nifedipine.

51

classification
Benzothiazepine derivatives Diltiazem Phenylalkylamine derivatives Verapamil Substituted dihydropyridines Amlodipine,felodipine,isradipine,nicardipine,nifedipine, oxodipine,nimodipine,nisoldipine.

52

Clinical manifestations
Interdental papilla-nodular and lobulated appearance Limited to attached and marginal gingiva

Anteriorly ,on facial surfaces.

Has been reported around dental implants. Does not effect edentulous patients

53

Pathogenesis
Ability to affect the calcium metabolism. Effects the cell proliferation, DNA synthesis and collagen synthesis Factors affecting the enlargement- dosage, age, duration of medication , length of time taken, sequestration of the agent in the GCF. Reduction in the cytosolic calcium levels in gingival fibroblasts

54

Nifedipine, one of the most commonly used .

Barclay (1992) gingival enlargement in 20% of the cases. Diltiazem , felodipine, nitrendipine and verapamil also induce gingival enlargement .

55

 The dihydropyridine derivative isradipine can in some cases replace nifedipine and does not induce gingival overgrowth. Nifedipine is also used with cyclosporine in kidney transplant recipients,

Bokenkamp(1994) concluded that the combined use of both drugs induces larger overgrowths . Nifedipine induced enlargement has been induced experimentally in rats where it appears to be dose dependent.

56

Other calcium channel blockers

Diltiazem Verapamil Steele et al (1994)compared 115 patients taking calcium antagonists with medicated controls,reported gingival enlargement prevalence of 21% with diltiazem and 4 % in controls.

57

Other drugs Vigabatrin is a relatively new medication used in the treatment of epilepsia

Katz et al(1997) reported the first enlargement in an19 year old woman. Cannabis: Gingival enlargement has also been described by case reports in individuals using Cannabis (marijuana) to excess. Gingivitis and alveolar bone loss may also occur in affected areas.

58

Erythromycin Yusok (1989) Association with administration of the antibiotic , erythromycin , in a 6 year old boy being treated for tonsillitis. The overgrowth became evident 1 week after initiation of the drug. Overgrowth involved anterior facial interdental papillae and the palatal and mandibular lingual gingiva.

59

Gingival enlargement not present

Patient taking drug known to cause enlargement

Gingival enlargement present

oral hygiene reinforcement professional recall enlargement regresss reevaluation

oral hygiene reinforcement Chlorhexidine gluconate rinse SRP Drug substitute Professional recall enlargement persists

Maintain good oral hygiene professional recall

gingivectomy Maintaenance Mouthrinse recall pressure appliance

Small areas of enlargement No attachment loss Horizontal bone loss Abundance of keratinized tissue

Periodontal surgery indicated

Large areas of enlargement Ossous defects Limited keratinized tissue Periodontal flap
60

Consider periodic surgical treatment

Idiopathic Gingival enlargement Rare condition of undetermined cause. gingivomatosis, elephantiasis, idiopathic fibromatosis, hereditary gingival hyperplasia and congenital familial fibromatosis. Clinical features. Affects the attached gingiva as well as the gingival margin and the interdental papilla The facial and lingual surfaces of the mandible and maxilla are generally affected, Enlarged gingival is pink, firm, and almost leathery in consistency. A characteristic minutely pebbled surface.

61

62

Histopathology Increase in the amount of connective tissue that is relatively

avascular Consists of densely arranged collagen bundles and numerous fibroblasts. surface epithelium is thickened and acanthotic with elongated retepegs.

63

Etiology
Hereditary basis The cause is unknown. Studies have found the mode of inheritance to be autosomal recessive in some cases and autosomal dominant in others.

64

 Kilpinen etal (1974) found that in some families, gingival enlargement may be linked to retardation of physical development. begins with the eruption of the primary or secondary dentition may regress after extraction, bacterial plaque is a complicating factor. Thomas etal (1994), gingival enlargement has been desribed in tuberous sclerosis, which is an inherited condition characterized by a triad of epilepsy, mental deficiency and cutaneous angiofibromas.

65

Systemic diseases causing gingival enlargement.

Conditioned Enlargements includes hormonal conditions ( eg-pregnancy, puberty), nutritional diseases such as vitamin C deficiency and some cases in which systemic influences is not identified. (Nonspecific conditioned enlargement)
Manifestation of the systemic disease independently of the inflammatory status of the gingival. This group come under systemic diseases causing gingival enlargement

66

Enlargement in Pregnancy

marginal , generalized or single or multiple tumour like masses. increase in the levels of progesterone and estrogen
hormonal changes vascular permeability leading to gingival edema , an increased inflammatory response to dental plaque. changes in subgingival microbiota

67

Marginal enlargement ; 10 % to 70% . presence of bacterial plaque. Clinical features. Varies considerably. Usually generalized and tends to be more prominent interproximally than on the facial and lingual surfaces . Enlarged gingival is bright red, magenta , soft and friable and has a smooth , shiny surface. Bleeding occurs spontaneously or on slight provocation.

68

Tumour like gingival enlargement Also called as the pregnancy tumour. ,epulis granulomatosum, granuloma gravidarum Is an inflammatory response to bacterial plaque modified by the patients condition. Usually appears after 3rd month of pregnancy but may occur earlier. Reported incidence is 1.85-5%

69

Clinical Features

discrete mushroom like, flattened spherical mass that protrudes from the gingival margin or more commonly from the interproximal space Is attached by a sessile or pedunclated base. expand laterally. Pressure from the tongue dusky red or magenta. smooth glistening surface numerous deep red, pinpoint markings. superficial lesion Consistency varies . painless

70

Histopathology
central mass of connective tissue ,. moderately fibrous stroma varying degrees of edema and chronic inflammatory infiltrate. epithelium is thickened , with prominent retepegs and some degree of intracellular and extracellular edema, prominent intercellular bridges, and leukocytic infiltration.

71

72

Gingival enlargement in puberty

Clinical Features prominent bulbous interproximal papillae. Often only the facial gingivae are enlarged, and the lingual surfaces are relatively unaltered. Gingival enlargement during puberty has all clinical features associated with chronic inflammatory gingival enlargement. After puberty the enlargement undergoes spontaneous reduction but does not disappear until plaque and calculus are removed.

73

 Sutcliffe etal (1972) conducted a longitudinal study of 127 children 11 to 17 years of age showed a high initial prevalence of gingival enlargement that tended to decline with age. Mombelli etal (1990) conducted a longitudinal study of subgingival microbiota of children between the ages of 11 and 14.and their association with clinical parameters has implicated capnocytophaga species in the initiation of pubertal gingivitis.

74

Histopathology Similar to that of chronic inflammation and prominent edema and associated degenerative changes.

75

Enlargement in Vitamin C deficiency

hemorrhage , collagen degeneration and edema of the gingival connective tissue. response of gingival to plaque scurvy. Clinical features marginal , bluish red, soft, friable, and has a smooth , shiny surface.Hemorrhage , occurring either spontaneously or on slight provocation and surface necrosis with pseudomembrane formation.

76

 Histopathology chronic inflammatory cellular infiltration with a superficial acute response. scattered areas of hemorrhage , engorged capillaries. diffuse edema , collagen degeneration and scarcity of collagen fibrils or fibroblasts are striking findings.

77

78

Contd.

79

PLASMA CELL GINGIVITIS : (Atypical Gingivitis And Plasma Cells Gingivostomatitis )

Etiology : Allergic in origin (like chewingum, dentifrices or various diet component). Clinical features :

More frequent in women and young adult.

It is located on the oral aspect of attached gingiva and therefore differs from plaque induced gingivitis.

PLASMA CELL GINGIVITIS

Symptoms : Patients may complain of a sore and burning mouth, scaling of lips and angular chelitis.

Entire free or attached gingiva is edematous, friable, granular, bright red

and bleeds on slightest provocation. Tongue is devoid of papillae and is erythematous.

An associated cheilitis and glossitis has been reported by Kerr (1971) and
Serio (1978 ) HISTOPATHOLOGY : Oral epithelium shows spongiosis and infiltration with inflammatory cells. Ultrastructurally there are signs of damage in the lower spinous layers and the basal layers. Underlying tissue contains a dense infiltrate of plasma cells.

NON SPECIFIC CONDITIONED ENLARGEMENT (Pyogenic Granuloma)

Pyogenic granuloma is a tumourlike gingival enlargement this is considered as exaggerated conditioned response to minor trauma.

Etiology
1. 2. 3. Microorganism : staphylococci, streptococci Trauma Local irritant : it is an inflammatory response to local irritation such as calculus. 4. Hormonal imbalance

Clinical features : Female are affected more than male with common age of occurrence 11-40 yrs. Its size ranges from 0.9- 2 cm. Asymptomatic, may be Papular or nodular Polypoid mass. Lesions are elevated pedunculated or sessile masses with smooth lobulated or even warty. Surface is commonly ulcerated and shows tendency to hemorrhage upon slightest pressure or trauma. Variegated red and white pattern. It may become mature and becomes less vascular and more collagenous

gradually converting into a fibrous epulis.

Histopathology mass of granulation tissue with chronic inflammatory cellular infiltration . Endothelial proliferation and the formation of numerous vascular spaces are prominent features.

The surface epithelium is atrophic in some areas and hyper plastic in others. Surface ulceration and exudation are common features. Treatment Removal of lesion, elimination of irritating factors .Bhaskar (1988) reported that the recurrence rate of pyogenic granuloma is 15%.
85

LEUKEMIA : Leukemic enlargement may be diffuse or marginal localized or

generalized.
it occur due to infiltration of malignant cells into the gingival tissue. The gingiva becomes soft, edematous and swollen. Appearance of gingiva is purplish and glossy.

There is also pallor in the surrounding mucosa.

Ulceration pain and severe hemorrhage can also occur. It has a spongy consistency and bleeds frequently.

LEUKEMIC ENLARGEMENT

Histopathology

Dense mass of immature and proliferating leukocytes. Engorged capillaries.

Edematous and degenerated connective tissue and epithelium Areas of acute necrotizing inflammation with pseudomambranous meshwork of fibrin. Necrotic epithelial cells, polymorphonuclear neutrophils (PMNS) and bacteria are often seen.

88

WEGENERS GRANULOMATOSIS

It is a rare disease characterized by acute granulomatous necrotizing lesions of the respiratory tract, including nasal and oral defects. Renal lesions develop and acute necrotizing vasculitis affects the blood vessels. It involve the orofacial region and include oral mucosal ulceration, gingival enlargement, abnormal tooth mobility, exfoliation of teeth, and delayed healing response.

Strawberry gums appearance of the mandibular gingiva is commonly seen.

 oral mucosal ulcerations , gingival enlargement , abnormal tooth mobility, exfoliation of teeth and delayed healing response. Granulomatous papillary enlargement is reddish purple and bleeds easily on stimulation. but the condition is considered an immunologically mediated tissue injury.

90

SARCOIDOSIS
It is granulomatous disease of unknown etiology. It starts in individuals in their 20s or 30s. predominantly affects blacks, and can involve almost any organ, including the gingiva, where a red, smooth, painless enlargement may appear. Enlargement is red , smooth and painless

Histopathology
Discrete , non seating whorls of epitheloid cells Multinucleated foreign body type giant cells Peripheral mononuclear cells.

92

NEOPLASTIC ENLARGEMENT (GINGIVAL TUMORS)

1. Benign tumors of the gingiva

2. Malignant tumors of the gingiva 1. BENIGN TUMORS OF THE GINGIVA
Epulis is a general term used clinically to designate all discrete tumors and tumor like masses of the gingiva. Neoplasms account for comparatively small proportion of gingival enlargement and make up a small percentage of the total number of oral neoplasms. In a survey by McCarthy(1941) of 257 tumours, approximately 8% occurred on the gingiva. In the study by Bernik in 1948 of 868 growths of gingiva and palate 57% were neoplastic and remainder inflammatory following incidence of tumor was noted.

Carcinoma-11% Fibroma -9.3% Giant cell tumour -8.4% Papilloma-7.3% Leukoplakia 4.9% Mixed tumour (salivary gland type-2.5%, Angioma-1.5%, Osteofibroma-1.3%, Sarcoma-0.5%, Melanoma-0.5% Myxoma-0.45%, Fibropapilloma-0.4%, Adenoma-0.4%, Lipoma-0.3%
94

FIBROMA
Fibromas of the gingiva arise from the gingival connective tissue or from the periodontal ligament. They are slow growing, spherical tumors that tend to be firm and nodular but may be soft and vascular. Clinical features : Common in 3rd, 4th and 5th decades. Usually painless, but if bitten or injured, there may be pain and discomfort. Sessile dome shaped or slightly pedunculated with smooth contour. There is no alteration in the colour of the gingiva.

Size of enlargement is usually very small but in rare instances may range upto several centimeters in diameter.
soft and myxomatous to firm and elastic consistency. According to the consistency, the tumor is termed as hard fibroma and soft fibroma.

Histopathology Fibromas are composed of bundles of well formed collagen fibers with a scattering of fibrocytes .

PAPILLOMA

Papillomas are benign proliferations of surface epithelium associated with the human papillomavirus (HPV).
Viral subtypes HPV-6 and HPV-11 have been found in most cases of oral papillomas.

CLINICAL FEATURES : Average age of occurrence is in the 3rd and 4th decades of life, only 20 percent cases are found below 20 yrs of age. The lesion appears solitary, wartlike or cauliflower like protuberances. They may be small and discrete or broad, hard elevations with minutely irregular surfaces. Size may vary around 2mm, but it is seldom larger than 2 cms. Tumor with much keratinization is white in color and lesion without much keratinization are grayish pink in color. Consistency is firm when keratinized and soft when non keratinized.

HISTOPATHOLOGY
The papilloma lesion consists of finger like projections of stratified squamous epithelium, often hyperkeratotic with a central core of

fibrovascular connective tissue.

GIANT CELL GRANULOMA Types: Peripheral giant cell granuloma it involves gingiva and alveolar mucosa. Central giant cell granuloma occurs as an endosteal lesion in the jaw bones. Peripheral Giant Cell Granuloma Also called as peripheral giant cell reparative granuloma, giant cell

epulis, osteoclastoma and peripheral giant cell tumor.

Etiology Injury may be caused by tooth extraction and dental irritation. Chronic Infection Hormonal increased circulating parathormane i.e. primary and secondary hyper parathyroidism.

Clinical features : Above 20 years of age, with an average of 45 yrs.

Females are affected twice as common as males.

Vary in appearance from smooth, regularly outlined masses to irregularly shaped, multilobulated protuberances with surface indentations.

Predominant in white persons. Ulceration of the margin is occasionally seen. The lesions are painless, vary in size and may cover several teeth. They may be firm or spongy. Color varies from pink to deep red or purplish blue. Microscopic examination is required for definitive diagnosis.

Histopathology
foci of multinuclear giant cells hemosiderin particles in a connective tissue stroma. Areas of chronic inflammation acute involvement at the surface. overlying epithelium -hyperplastic.

Central Giant cell granuloma : These lesions arise within the jaws and produce central cavitation. They occasionally create a deformity of the jaws that makes the gingival appear enlarged.

103

LEUKOPLAKIA Defined by the WHO as a white patch or plaque that does not rub off and cannot be diagnosed as any other disease. Etiology:

Local factors :
Tobacco Alcohol Chronic irritation Candidiasis

Regional or systemic factors :

Syphilis Vitamin deficiency

Nutritional deficiency Xerostomia

Hormones
Drug Anticholinergic Antimetabolic Systemically administered alcohol

Virus Herpes simplex Human papilloma virus.

LEUKOPLAKIA

CLINICAL FEATURES : Occurs more commonly in older age group i.e. 35-45 yrs and above. Males are affected more frequently than females.

Prevalence in India is 0.2 to 4.9 percent

Gingiva varies in appearance from a grayish white, flattened, scaly lesion to a thick, irregularly shaped keratinous plaque.

HISTOPATHOLOGY : Leukoplakia exhibits hyperkeratosis and acanthosis, premalignant and malignant cases have a variable degree of atypical epithelial changes that may be mild, moderate, or severe, depending on extent of involvement of the epithelial layers.
Dysplastic changes involve all the layers , it is diagnosed as a carcinoma in situ.

Gingival Cyst

Gingival cysts of microscopic proportions are common Seldom reach a clinically significant size Appear as localized enlargements Involves marginal and attached gingiva. Occur most often on the lingual surface of mandibular canine and premolar areas. Develops from odontogenic epithelium or sulcular epithelium uneventful recovery.

108

Histopathology Lined by thin , flattened epithelium with or without localized area of thickning. Less frequently, following types of epithelium can be found: unkeratinised stratified squamous epithelium, keratinized stratified squamous epithelium and parakeratinised epithelium with palisading basal cells. Other benign tumours also have been desribed as rare or infrequent findings in the gingiva. They include nevis, myoblastoma hemangioma, neurilemoma, neurofibroma, mucus secreting cysts (mucoceles) amd ameloblastoma.

109

MALIGNANT TUMORS OF THE GINGIVA CARCINOMA Clinical features: Common in 5th and 6th decade of life. Carcinoma of mandibular gingiva is more common than maxillary gingiva. More commonly arise in edentulous area. The fixed gingiva is invaded more than the free gingiva. It usually occurs in premolar area.

In maxilla, gingival carcinoma after invades maxillary sinus or it may extend to palate or tonsillar pillars.
It is manifested as an area of ulceration, which may be a purely erosive lesion and may exhibit an exophytic, granular or verrucous type of growth. Quickly spreads from gingiva to alveolar bone.

CARCINOMA

MALIGNANT MELANOMA :

Malignant melanoma is a rare oral tumor that tends to occur in the hard palate
and maxillary gingiva of older persons. It is usually darkly pigmented and is often preceded by localized pigmentation.

It may be flat or nodular and is characterised by rapid growth and early

metastasis. It arises from melanoblasts in the gingiva, cheek, or palate. Infiltration into the underlying bone and metastasis to cervical and axillary lymph nodes are common. Sarcoma Kaposis sarcoma often occurs in the oral cavity of patients with acquired immunodeficiency syndrome (AIDS), particularly in the palate and the gingiva.

Metastasis Metastasis has been reported with various tumors, including adeno carcinoma of the colon, lung carcinoma, primary hepatocellular carcinoma, renal cell carcinoma and testicular tumor.

FALSE ENLARGEMENT False enlargement are not true enlargement of the gingival tissues but may appear as such as a result of increase in size of the underlying osseous or dental tissues. UNDERLYING OSSEOUS LESIONS : Enlargement of the bone subjacent to the gingival area occur most often in tori and exostoses. It can also occur in pagets disease, fibrous dysplasia, cherubism, central giant cell granuloma, ameloblastoma, osteoma and osteosarcoma.

UNDERLYING DENTAL TISSUES During various stages of eruption particularly of the primary dentition, the labial gingiva may show a bulbous marginal distortion caused by superimposition of the bulk of the gingiva on the normal prominence of the enamel in the gingival half of the crown. This enlargement has been termed developmental enlargement. Developmental gingival enlargements are physiologic and usually presents no problems until when it is complicated by marginal inflammation which leads to extensive gingival enlargement.

Treatment of chronic inflammatory enlargement

scaling and rootplaning , surgical removal is the treatment of choice. Gingivectomy flap operation. Tumour like inflammatory enlargements are treated by gingivectomy.

115

Treatment of Periodontal and Gingival Abscesses Acute Periodontal Abscess allevate the pain, control of spread of infection, establish drainage. proper antibiotic regimen started if necessary. Drainage through pocket external incision from the outer surface..

116

Treatment of Gingival Abscess

Under topical and local infiltrative anaesthesia , the fluctuant area of the lesion is incised with a # 15 blade, and the incision is gently widened to permit drainage . The area is cleansed with warm water and covered with a gauze pad . After bleeding stops, the patient is dismissed for 24 hours and instructed to rinse every 2 hours with a glassful of warm water . After 24 hrs topical anaesthetic is applied , and the area is scaled . If the residual size of the lesion is too large , it is removed surgically.

117

Treatment of drug induced gingival enlargement

Alternative medications phenytoin -carbamezipine. valproic acid nifedipine -other calcium channel blockers such as diltiazem or verapamil another class of antihypertensive medications rather than calcium channel blockers,

118

 cyclosporine -tacrolimus. There is also preliminary evidence that the antibiotic azithromycin may aid in decreasing the severity of cyclosporine induced gingival enlargement. plaque control as the first step in the treatment of drug induced gingival enlargement. Also , adequate plaque control may aid in preventing or retarding the recurrence of gingival enlargement.in surgically treated cases. surgery , either gingivectomy or the periodontal flap.

119

Treatment Of Leukemic Enlargement

Treatment of acute symptoms, correction of the gingival enlargement. remove the local irritating factors to control the inflammatory component of the enlargement.. scaling and rootplaning chlorhexidiene mouth washes. Oral hygiene procedures. Progressively deeper scalings. confined to a small area Antibiotics
120

Treatment of gingival enlargement in pregnancy

scaling and curettage. surgical excision and scaling and planning of tooth surfaces. the enlargement recurs unless all irritants are removed. Food impaction is frequently an inciting factor

121

 Treatment of Gingival Enlargement in Puberty. performing scaling and curettage , removing all sources of irritation and controlling plaque. Surgical removal may be required in severe cases. recurrence due to poor oral hygiene.

122

Conclusion
Gingival enlargement is a common clinical entity and classified in to different types according to the etiological factors and underlying pathological process.It is not always possible to identify the exact etiological factors responsible for such enlargement and classify them in to a particular type .The treatment has to be planned after taking a thorough examination and recording necessary investigations. It includes plaque control, scaling and rootplaning, flap surgery , surgical exision,gingivoplasty and gingivectomy.

123

 References:
1)Clinical Periodontology Carranza, Takei, Newman. 10th edition.
2)Thorkild Karring, Jann Lindhe and Pierpaolo Cortellini. Regenerative Periodontal Therapy; Clinical Periodontology; Jan Lindhe 5th edition.. 3)Schafers text book of Oral pathology 5th edition 4)Treatment of drug induced gingival enlargement : aesthetic and functional considerations: Periodontology 2000,Vol 27,2001 ,131-138 5) esentials of medical pharmacology- K D tripathi; 5th edition

6) Ayanoglou CM, Lesty C: Cyclosporin A induced gingival enlargement in rats : A histological , ultra structural and histomorphometric evaluation,. J Periodont Res 1999;34;7-15
124

 7) Barak, S, Egelberg IS: Gingival enlargement caused by Nifedipine. Histological findings. J Periodontol 1987;8:639-642 8) Cockey G, Boughman I, Hassel T:Phenytoin induced response of gingival fibroblasts from human twins . J Dent Res 1987:66:320 9)Diagnosis of Periodontal manifestations of systemic diseases. Periodontology 2000 Vol 34, 2004 217-229. 10) Drugs and oral disorders Periodontology 2000 ,Vol18,1998,21-36. 11)Journal of Clinical PeriodontologyVolume 21 Issue 4 Page 256-259, April 1994

125