GINGIVAL ENLARGEMENT

BY ROHAN SHAH RONAK SHAH MILIND SHAH

YASH DAWAWALA

 Usually caused by local conditions such as poor oral hygiene, food impaction, or mouth breathing. Systemic conditions such as hormonal changes, drug therapy, or tumor infiltrates may complicate the process When edema, vascular engorgement, and inflammatory cell infiltration predominate, gingival enlargement is referred to as inflammatory gingival hyperplasia. Examples: local irritants; therapy with anticonvulsants, calcium channel blockers, and immunosuppressive medications; pregnancy ; monocytic leukemia; and clinical scurvy , congential epulis, phenytoin-induced hyperplasia, pyogenic granuloma, leukemic gingival enlargement, diabetic gingivitis, scurvy, and some of the congenital and inherited gingival enlargements.

According to etiology and pathology Acute Chronic Drug induced idiopathic C. Combined enlargement (inflammatory + fibrotic) B. Fibrotic enlargement A. Inflammatory

D. Enlargement associated with systemic diseases

1)Conditional enlargement pregnancy Puberty Plasma cell gingivitis 2)Systemic diseases causing gingival enlargement Leukemia

Crohn`s disease Wegener`s granulomatosis Vitamin c deficiency E. Neoplastic enlargement Benign tumor Malignant tumor F. False enlargement

INFLAMMATORY GINGIVAL ENLARGEMENT

In most instances, inflammatory gingival enlargement begins at an area - poor oral hygiene - food impaction, or - other local irritation that can be readily controlled. However, the pseudo pockets formed by gingival enlargement make the maintenance of good oral hygiene difficult, perpetuating a cycle of inflammation and fibrosis.
. The involved tissues are - glossy, - smooth, and - odematous and - bleed readily. A fetid odor may result from 1. the decomposition of food debris and 2. from the accumulation of bacteria in these inaccessible areas Loss of interseptal bone and drifting of the teeth occur in long-standing cases of inflammatory enlargement. These changes are commonly referred to as gingivitis, or periodontal disease when the process involves the loss of gingival attachment and the subsequent loss of interproximal bone

 Gingival inflammation affecting primarily the maxillary anterior region is observed in mouth breathers In some patients, - abnormal facial development or -malocclusion leads

to a continued opening of the mouth

which predisposes these patients to this form of gingivitis

 Varying degrees of gingival hyperplasia probably due to hormonal changes have. been observed in association with the use of contraceptive pill The diagnosis of inflammatory gingival enlargement usually presents no difficulty - The edema of the tissues, - their bright red or purplish red color, and - their tendency to hemorrhage permits ready differentiation from fibrotic gingival enlargement. Although most gingival enlargements are inflammatory in nature, benign and malignant neoplasms of the gingivae also occur. A biopsy should be performed whenever the cause is unclear or whenever the lesion does not respond to local therapy

HISTOLOGIC FEATURES
acute inflammation ;- the surface epithelium has varying degree of edema - purulent focus in the connective tissue surrounded by diffuse infiltration of the PMNs leuckocytes ,edematous tissue

Chronic inflammation; - shows exudative and proliferative features of the chronic inflammation - lesion may contain preponderance of inflammatory cells and fluid with vascular engorgements ,new capillary formation.

TREATMENTS

Treatment of the inflammatory type of gingival enlargement consists of - the establishment of excellent oral hygiene, - the elimination of all local predisposing factors if possible, the - elimination of any recognized systemic predisposing causes, and - proper home care by the patient. In patients with extensive gingival hyperplasia the affected tissue must be removed surgically and the remaining tissue must be properly contoured
All local irritative factors such as calculus, the margins of cervical cavities or areas of food impaction should be corrected The successful treatment of gingival enlargement in mouth breathers depends mainly on the elimination of the habit Referral to an otolaryngologist (to determine if there is some obstruction of the upper air passages, such as enlarged adenoids ) or orthodontic treatment may be required to permit the normal closure of the lips during Protective ointment such as Vaseline or Orabase may be applied to the gums at night

Fibrotic Gingival Enlargement

Gingival lesions of the fibrotic type have a normal pink color, or they may be slightly paler than normal The tissue is firm, hard, and fibrous in consistency (because of the increase in fibrous tissue) and does not bleed readily or pit on pressure Typical examples of gingival fibrosis are found in the gingival enlargements associated with the administration of the immunosuppressant cyclosporine, several calcium channel blocking agents, or phenytoin (Dilantin) and its derivatives and in diffuse fibromatosis of the gingiva. A fibrotic gingival enlargements occurs in any patients with long-standing gingival hyperplasia

Phenytoin Sodium
Clinical features Gingival hyperplasia may begin as early as two weeks after dilantin therapy. Site the hyperplasia is generalized throughout the mouth, but it is most severe in maxillary and mandibular anterior region.

Appearance
- The first change noted is a painless bead like enlargement in the size of the gingiva, starting with one or two interdental papillae. - The surface of gingiva shows an increasein stippling. - As the enlargement increases, the gingival tissue becomes lobulated and clefts are seen. Palpation reveals that the tissue is dense, resilient and insensitive.

The presence of an enlargement makes plaque control difficult, resulting in a secondary inflammatory process that complicates the gingival hyperplasia.

Histopathological features
The stratified squamous epithelium covering the tissue is thick and has a thin keratinized layer. The rete pegs are extremely long and thin, sometimes called as test tube pegs.

The bulk of tissue is made up of large bundles of fibers, interspersed with fibroblasts and fibrocytes.
There may be a pronounced hyperplasia of the connective tissue and the epithelium.

Management
If hyperplasia interferes with function, surgical excision is recommended. Discontinuing the drug will result in gradual diminution of the bulk of the gingiva.

Gingival Hyperplasia Induced by Cyclosporin A and Calcium Channel Blockers

For more than 40 years, phenytoin and its derivatives were the only
drugs that were known to be associated with gingival hyperplasia. In the last 10 years, however, two new classes of drugs, the immunosuppressant cyclosporine308 and several calcium channel calcium channel blockers developed for treatment of hypertension and hypertensive cardiovascular disease, have been shown to have similar effects clinically, in experimental animals and in vitro The changes that are produced by these new agents are very similar to changes that are associated with phenytoin therapy although differences in the latent period for the development of gingival changes have been described. Two of the calcium channel blockers (oxodipine and nifedipine) also appear to cause hyperplasia of the labial mandibular gingiva rather than generalized gingival enlargement314 although this phenomenon may reflect species and dose rather than specific drug effects.

In comparison with phenytoin-induced gingival hyperplasia, hyperplasia caused by calcium channel blockers (both substituted dihydropyridines and verapamil) is probably of low incidence but is similarly dose dependent (with nifedipine, 48 mg/d produced gingival hyperplasia whereas 35 mg/d did not)312 and positively correlated with oral hygiene and with the degree of gingival inflammation. Phenytoin, cyclosporine A, and the substituted dihydropyridines are chemically dissimilar compounds, and no common metabolic breakdown product that might serve as a common denominator has been identified.

However, all three influence calcium/sodium (Ca++/Na+) flux, and this effect has been proposed as the common mechanism for development of the gingival hyperplasia associated with the three classes of drug

Because folic acid is actively taken up at the cellular level by a Na+-dependent transport mechanism, the effect of these three drugs on folic acid metabolism is being investigated Two other findings associated with the gingival hyperplasia induced by these newer agents may provide new avenues

for investigating the long-recognized but poorly understood phenomenon of druginduced gingival overgrowth. These are the production of gingival hyperplasia without inflammatory
changes in rats treated with the experimental drug oxodipine314 and the recognition of ultrastructural myofibroblastic modification of over 20% of the fibroblasts in human cyclosporine-induced hyperplastic gingiva

Profile and intraoral appearance of a 49-year-old male before all visible and easily accessible teeth were removed, after which he was able to appose his lips for the first time in his life. Gingivae had been resected several times before. The father, son, and daughter all suffered from hereditary gingivofibromatosis.

Pronounced gingival hyperplasia in this 12-month-old child is associated with mucolipidosis II (I-cell disease).

Hyperplasia, developed during the first year of life and before the eruption of deciduous dentition. This hyperplasia was noted in association with multiple developmental abnormalities, skeletal changes (similar to those of Hurlers syndrome) in the lower limbs and pelvis, unusual facies, and psychomotor retardation. The enlarged gingival tissue was firm and hard and obstructed mastication and closure of the mouth.

Fibroblasts cultured from the skin biopsy specimen, showing numerous granular inclusions and the complete absence of lysosomal -galactosidase activity.

Electron microscopic examination of gingival fibroblasts shows numerous membrane-limited empty vacuoles distending these cells.

ENLARGEMENT IN PREGNANCY: It can be marginal or generalized Single or multiple tumor like masses C/F:Marginal enlargement: More prominent interproximally than on facial surface Bright red color, soft and friable and smooth surface Bleeding occurs on provocation

Pregnancy tumor: It is an inflammatory reaction to local irritants and appears after 3rd month of pregnancy. The lesions appears as discrete, spherical masses that protrude from gingival margins. It is dusky red colored. Has smooth glistening surface Usually painless. But accumulation of food debris or intereference with occlusion may cause pain. H/F: central mass of connective tissue with periphery of stratified squamous epithelium Prominent rete pegs Connective tissue consists of numerous newly formed and engorged capillaries. Between the capillaries there is varying degree of edema and leukocytic infiltration. Management: Most gingival enlargement during pregnancy can be prevented by removal of local irritants.

ENLARGEMENT IN PUBERTY:

Associated with inflammatory type.

C/F: Involves mainly marginal gingiva and interdental gingiva Characterized by prominent interproximal papillae. Sometimes only facial gingiva are enlarged After puberty the enlargement undergoes reduction but does not disappear until irritants are removed. H/F: Chronic inflammatory cells with prominent edema and associated degenerative changes.

PLASMA CELL GINGIVITIS: (Atypical gingivitis or atypical gingivostomatitis) Allergic in origin and caused by some ingredients in chewing gums, dentifrices or diet components Site: located on oral aspect of attached gingiva Symptoms: patient complains of burning mouth, scaling of lips and angular chelitis Appearance: entire free and attached gingiva is edematous, friable, bright red and bleeds on provocation.

Management: cessation of exposure to allergen resolves the lesion.

GRANULOMA PYOGENICUM: Nonspecific, tumor-like, conditional enlargement of the gingiva as an exaggerated response to minor trauma C/F: Appears as discrete spherical tumor-like mass with a pedunculated attachment Presents with surface ulceration and purulent exudation.

H/F: Appears as mass of granulation tissue with chronic inflammatory cell infiltration Surface epithelium is atrophic Management: Removal of lesion Elimination of irritating factor.

H/F: Appears as mass of granulation tissue with chronic inflammatory cell infiltration Surface epithelium is atrophic Management: Removal of lesion Elimination of irritating factor.

Systemic diseases causing enlargement

Leukemia
Occurs due to infiltration of malignant cells. Gingiva becomes soft, edematous, swollen, purpalish, glossy. Pallor in surrounding mucosa. Ulcerations, pain, bleeding occurs.

Crohns disease
Characterized by granulamatous superficial ulceration of intestinal epithelium. Appears as granular, erythamatous swelling. Other oral features include Cobble stone appearance of buccal mucosa, indurated swelling of lips & ulcerations of palate.

Vit. C deficiency
Gingiva becomes tender, edematous, swollen. It has spongy consistency, & bleeds frequently. The crest of interdental papilla appears red, or purple

Orofacial Angiomatosis
Gingiva appears red & swollen. False gingival pocket can occur. Angiomatous proliferation of blood vessels may cause gingival hyperplasia

Wegeners Granulomatosis
Focal gingival swelling can occur. It is characterized by epithelial proliferation & dense inflammatory cell infiltration

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