TREATMENT OF GINGIVAL ENLARGMENTPresented by,Dr Harshavardhan Patwal

Gingival enlargement, is increase in the size of the gingiva. Epulis is a generic term used to designate all discrete tumors and

tumor-like masses. Hypertrophy- is an increase in the size of the cells, resulting in

increase in the size of the organ. Hyperplasia- is an increase in the number of cells, resulting in

increase in the size of the organ. Atrophy- shrinkage in the size of the cell by the loss of cell

substance. Ephelides are sun-induced freckles, which are small light to dark

brown macule that appears on the skin or lips.

Gingival enlargement can be classified, according to etiologic factors and pathologic changes as follows:

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 deficiency

4. Plasma cell gingivitis

5. Nonspecific conditioned enlargement (granuloma

pyogenicum)

B. Systemic diseases causing gingival enlargement

1. Leukemia

2. Granulomatous diseases (Wegener’s granulomatosis,

sarcoidosis)

IV. Neoplastic enlargement (gingival tumors)

A. Benign tumors

B. Malignant tumors

V. False enlargement

Using the criteria of location and distribution, gingival

enlargement is designated as follows:

Localized: Limited to the gingiva adjacent to a single tooth or

group of teeth.

Generalized: Involving the gingiva throughout the mouth.

Papillary: Confined to the interdental papilla.

Diffuse: Involving the marginal and attached gingivae and papillae

Discrete: An isolated sessile or pedunculated tumor like enlargement

Treatment of gingival enlargement is based on an understanding of the cause and underlying pathologic changes.

Gingival enlargement is of concern because they pose problems in plaque control, function and esthetics.

CHRONIC INFLAMMATORY ENLARGEMENT: Chronic inflammatory enlargements, which are soft and

erythematous and are caused principally by edema and cellular infiltration are treated by scaling and root planing, provided the size of the enlargement does not interfere with complete removal of deposits from the involved tooth surfaces.

When these inflammatory enlargements include a fibrotic component, surgical removal is the treatment of choice.

Two techniques available for this purpose are- Gingivectomy and Flap operation.

Selection of the technique depends on the size of the enlargement and character of the tissue.

If the gingivectomy incision removes all the gingiva and creates a mucogingival problem then a flap operation is indicated.

Tumor like enlargements are treated by gingivectomy by seperating the lesion from the mucosa at its base. If the lesion extends interproximally, the interdental gingiva is included into the incision to ensure exposure of the irritating root deposits.

ACUTE INFLAMMATORY ENLARGEMENT:Definition: The periodontal abscess has been defined as a lesion with an expressed

periodontal breakdown, occurring during a limited period of time, and with easily detectable clinical symptoms(Hafstrom et al. 1994),with a localized accumulation of pus(dewitt et al. 1985, Carranza 1990),located within the gingival wall of the periodontal pocket(Carranza 1990).

Prevalence: The periodontal abscess was the third most prevalent emergency

infection, after acute dento-alveolar abscesses(14-25%), and pericoronitis(10-11%).

Teeth with an abscess are usually considered as hopeless(becker et al. 1984), and therefore the occurrence of an abscess may be one of the main reason for tooth extraction during periodontal maintenance (chace & low,McLeod et al. 1997).

Periodontal abscesses in periondontitis: In periodontitis, a periodontal abscess represents a period of active

bone destruction(exacerbation), although such events also occur without abscess formation. The exsistence of tortuous pockets, with cul-de-sac, which eventually become isolated, may favour the formation of abscesses(Carranza 1990).Fibrin secretions leading to the local accumulation of pus may favour the closure of gingival margin to the tooth surface(Galego-Feal et al. 1995). Changes in the composition of the microflora, bacterial virulence, or in host defences(Kareha et al.1981) could also make the pocket inefficient to drain the increased suppuration.

The development of a periodontal abscess in periodontitis may occur at different stages during the course of the infection:as an acute exacerbation of an untreated periodontitis(Dello Russo 1985); during periodontal therapy((Dello Russo 1985, Carranza 1990); or during periodontal maintenance(Chase & Low 1993,McLead et al. 1997).

Treatment with systemic antibiotics without subgingival debridement in patients with advanced periodontitis may also cause abscess formation(Helovuo & Paunio 1989, Helovuo et al. 1993, Topoll et al. 1990).

Another systemic therapy that has been related to the development of multiple abscesses is nifedipine.

Periodontal abscesses in the absence of periodontitis: Periodontal abscess can also develop in the absence of periodontitis,

due to the following causes:

(a)impaction of foreign bodies(Kareha et al. 1981), such as an orthodontic elastic(Pini Prato et al. 1988), a piece of dental floss(Abrams &Kopczyk 1983), a popcorn kernel(Rada et al. 1987), a dislodged cemental tear(Haney et al. 1992), a piece of tooth pick(not confirmed)(Fuss et al.1986),a corn husk in peri-implant tissues(Ibbott et al. 1993), or a known object(Emsile, 1978, Palmer 1984). Periodontal abscess caused by foreign bodies, related with oral hygiene aids, have named “oral hygiene abscess”(Gillette & Van House 1980).

(b)perforation of the tooth wall by an endodontic instrument(Carranza 1990 , Abrams et al. 1992).

(c)infection of lateral cysts(Kareha et al. 1981).(d)local factors affecting the morphology of the root may predispose to

periodontal abscess formation.

PATHOGENESIS AND HISTOPATHOLOGY: The entry of bacteria into the soft tissue pocket wall could be the first

event to initiate periodontal abscess. Inflammatory cells are then attracted by chemotactic factors released by the bacteria , and the concomitant inflammatory reaction leads to destruction of the connective tissue(Dewitt 1985), the encapsulation of the bacterial infection and the production of pus(Carranza 1990)

DIAGNOSIS:

Diagnosis of a periodontal abscess is based on the symptoms revealed by the patients and the signs found during the oral examination. The current sign is an ovoid elevation of the gingiva along the lateral part of the root(Carranza 1990). Symptoms range from light discomfort to severe pain, tenderness of the gingiva, swelling , tooth mobility(Ibbott 1993). Another common finding is suppuration, either spontaneous or after pressure on the abscess ( Carranza 1990), combined with rapid tissue destruction and deep pocket formation (Ibbott 1993).

Periodontal abscesses classified in different ways:

Depending on the location of the abscess, they have been divided into periodontal and gingival abscess( Gillette & Van house 1980).

The gingival abscess is described as localized, painful swelling affecting only the marginal and interdental gingiva. The main ethiological factor is the impaction of foreign objects.

Histologically the lesions are identical, but the periodontal abscess occurs in a periodontal pocket related to destruction by periodontitis.( De Witt 1985), and in gingival abscess effects only the marginal soft tissues of previously healthy sites( De Witt 1985).

Depending on the course of the lesion, they have been divided into acute and chronic .( Galego- Feal 1995). The acute periodontal abscess usually demonstrates symptoms like pain, tenderness, sensitivity to palpation, suppuration upon gentle pressure.

Depending on the number they have been divided in single verses multiple periodontal abscess( Topoll 1990). Some lesions caused by patients habits can mimic periodontal abscess such as trauma of gingiva with pencil( Rodd 1995) or safety pin( Beckett 1995).

TREATMENT: In the 17th century, Louis XIV of France, was treated for his periodontal

abscesses with masses of mixed bread and milk, in order to soften the swelling, and to allow drainage of abscess( Gonzalez-Iglesias 1990).

The treatment of the acute periodontal abscess usually includes 2 stages: the management of acute lesion; and appropriate treatment of the original and/or residual lesion, once the acute situation is controlled( Ammons 1996). If the tooth is severely damaged with poor prognosis, extraction is the treatment of choice.( Smith & Davies 1986)

For the treatment of gingival abscess, should include the elimination of foreign object, through careful debridement( Abrams 1983), drainage through the sulcus with probe, rinsing with warm saline and follow-up after 24-48 hrs.

For the treatment of periodontal abscess, a similar protocol is : drainage through the pocket, scaling, compression and debridement of soft tissue wall and irrigation with sterile saline. 1 week later, the definitive treatment should be carried out( Ammons 1996).

Alternatively , drainage could need an external incision or flap, and topical antiseptics may be applied after the drainage(Carranza 1990).

The addition of systemic anti biotics to the treatment regime of the periodontal abscess is not a well defined issue. Some authours recommend the combination of basic treatments and antibiotic therapy(Galego-Feal 1995). The combination of incision and drainage with the systemic administration of penicilins has been considered as” often successful”(Genco 1991).

ANTIBIOTIC OPTIONS FOR PERIODONTAL INFECTIONS:

AMOXICILLIN, 500 mg•1 g loading dose, then 500 mg three times a day for 3 days.

•Reevaluation after 3 days to determine need for continued or adjusted antibiotic therapy.

PENICILLIN ALLERGYClindamycin •600 mg loading dose, then 300 mg four times a day for 3 days.

Azithromycin •1 g loading dose, then 500 mg four times a day for 3 days.

DRUGS ASSOCIATED WITH GINGIVAL OVERGROWTH:

Anticonvulsants Anticonvulsants

Hydantoins:Ethotoin

Mephenytoin

Phenytoin

Succinimides:Ethosuximide

Methsuximide

Phensuximide

Valproic acid

Immunosuppressants:Immunosuppressants: Cyclosporine A Calcium channel blockers:Calcium channel blockers: Dihydropyridine derivativesDihydropyridine derivatives Amlodipine Felodipine Nicardipine Nifedipine

Nimodipine Nisoldipine Nitrendipine

Benzothiazine derivatives:Benzothiazine derivatives:Diltiazem

Phenylalkylamine derivatives:Phenylalkylamine derivatives:Verapamil HCL

GRADING FOR GINGIVAL ENLARGEMENT:

Angelopoulos and Goaz classification

Grade 0- No gingival overgrowth

Grade 1- Overgrowth covering the cervical one third of clinical crown

Grade 2 -Overgrowth extending till the middle third of crown

Grade 3- Overgrowth covering the two thirds of crown or the whole of attached gingiva was affected

Bokenkamp classification (1994)

Grade 0- No sign of gingival enlargement Grade 1- Enlargement confined to interdental papilla Grade 2-Enlargement involving papilla and marginal gingiva Grade 3-Enlargement covering three quarter or more of crown

Hyperplastic index (Seymour et al 1985) Vertical or apicocoronal component Grade Criteria 0 no gingival hyperplasia 1 Blunting of gingival margin 2 Hyperplasia less than half of crown length 3 Hyperplasia more than half of crown length

Horizontal or labio-lingual component

1 Normal width of free gingival margin

2 Thickening from normal up to 2mm

3 Thickening from normal >2mm

ANTICONVULSANTS:

Phenytion (5-diphenyl phenytion) is an anticonvulsive drug

widely used in the control of epilepsy and other convulsive

disorders. It was first introduced by Merritt and Putnam in 1938.

It is also used in the management of trigerminal, glossopharyngeal

and post herpetic neuralgia and occasionally to treat ventricular

arrhythmias.

Within a year of its initial clinical use, reports linking phenytoin to

gingival enlargement appeared in the literature ( Kimball 1939)

Pharmacological actions:-

Mediated through depression of CNS motor cortex without any

significant effect on sensory regions ( Pincus et al 1970)

At cellular level, phenytoin is thought to act through suppression of

sodium-potassium ATP ase pump , therby diminishing the

hyperexcitability of affected neurons in motor cortex

It also has the ability to inhibit intracellular calcium uptake on which

ATP ase is dependant ( Seymour 1991)

Gingival overgrowth is the main side effect following the usage of phenytoin. Other unwanted effects of phenytoin include cardiac arrhythmias, depression of the CNS, drowsiness, hirsuitism and osteomalacia.

Reports of the incidence of phenytoin associated gingival overgrowth range from 0% - 84.5% , with an average effect approximating 50%.

In a longitudinal study , Dahlof and Modeer observed the clinical onset of gingival overgrowth after 1 month of phenytoin use.

The earliest signs of gingival change, soreness and tenderness start occurring 2-3 weeks after phenytoin therapy.

During the first 6-9 months, there is initial enlargement of the interdental papillae facially and lingually which is less frequently accompanied by increased thickening of the marginal tissue.

Affected papillae may become enlarged to the point that they contact, resulting in the clinical presence of pseudoclefts.

Overgrowth usually diminishes as it approaches the mucogingival junction, but coronal progression may partially or totally obscure the crowns of the teeth (Angelopoulos et al. 1972).

Affected tissues typically present a granular or lobulated surface .

The facial gingiva of the anterior sextants is more commonly affected

and often results in esthetic disfigurement (Butler et al. 1987)

The colour of the gingiva range from coral pink to a deep bluish red

depending upon the amount of inflammatory infiltrate present

(Esterberg and white 1945). Enlargement of the gingival tissues may

result in malpoistioning of teeth and interference with normal

masticatory function, speech and oral hygiene (Philstrom BL 1990).

CYCLOSPORIN: Cyclosporine is a new immunosuppressant discovered by Borel

(1997). The use of CsA is associated with significant side effects,

including nephropathy, hypertension, hepatotoxicity, thromboembolic complications, neurotoxicity, hypertrichosis, and gingival overgrowth . Gingival overgrowth is observed in 25% to 81% of patients undertaking CsA .

The first case of drug induced gingival overgrowth related to cyclosporin A medication was reported in 1981 (Starzl et,al.,) and confirmed later by Rateitschak- pluss 1983 in dental literature. Wysocki, T.D. Daley 1984 gave a report to familiarize the dental community, with cyclosporin and to discuss its anticipated impact on the practice of periodontics.

The swelling enlarges and adjacent papillae appear to coalesce giving the gingiva a lobulated appearance

Overgrowth is restricted to the width of the attached gingiva, but can extend coronally and interfere with the occlusion, mastication and speech and even cause migration of teeth

The hyperplastic gingiva often show marked inflammatory changes which bleed readily on probing and is more hyperemic than the phenytoin induced gingival overgrowth.

Cyclosporin A induced gingival overgrowth, when removed leads to spontaneous repositioning of migrated teeth as early as 2 months after surgery (Rostock et al. 1986).

The incidence of cyclosporin induced gingival overgrowth varies between 25-50% depending upon drug dosage, plasma concentration, duration of therapy, method of assessing gingival enlargement, underlying periodontal status, age of the patient, medical status and genetic predisposition to be responders or non responders.

A combined drug treatment consisting of Cyclosporin A along with calcium channel blockers of the Dihydropyridine derivatives has synergistic effects and is a significant risk factor for progression or recurrence of gingival overgrowth among susceptible patients (Slavin and Taylar, 1987, Pernu et al. 1993).

CALCIUM CHANNEL BLOCKERS:

All the agents of Ca+ channel blockers bring about similar clinical features of gingival changes. The hyperplasia appears shortly after the start of therapy and decreases on withdrawal of the drug (Lederman et al. 1984).

Calcium channel blockers act by inhibiting calcium ion influx across the

cell membrane of cardiac and smooth muscle cells thereby blocking the intracellular mobilization of Ca++. It causes dilatation of coronary arteries & arterioles as well as decreased myocardial contractility and oxygen demand. The first report of occurence of gingival overgrowth associated with calcium channel blocker (nifedipine) was reported by Ramon et al. 1984. Amilodipine, filodipine, diltazem, nitrendipine & Verapamil are the other agents associated with this side effect.

Ellis et al. 1993 suggest that very high concentrations of nifedipine may occur in GCF, which may favour the likelihood of toxic effects. On the contrary, Thomson et al. 1995 found no apparent relationship between GCF levels of the drug and the gingival changes.

The interdental papilla are initially affected, becoming enlarged

and resulting in a lobulated or nodular morphology. These

effects are limited to the attached and marginal gingiva, and are

more frequently observed anteriorly, especially on the facial

surfaces.

Management of drug-induced gingival overgrowth include:-

Non-Surgical Approaches - Scaling - Root planing - Antiseptic mouthwashes

- Systemic antibiotics - Change in medication

Surgical approaches - -- Scalpel Gingivectomy

Electrosurgery Laser Gingivectomy

- Flap Surgery

First- consider the possibility of changing or discontinuing the drug. This should be done with the consultation of the patient’s physician.

If any drug substitution is attempted, it is important to allow for a 6 to 12 month period of time to elapse between discontinuation of the offending drug and the possible resolution of gingival enlargement before a decision to implement surgical treatment is made.

Alternate mediation to phenytoin include Carbamezapine and Valproic acid,

Which have been reported to induce lesser gingival overgrowth.

For patients with nifedipine, induced gingival overgrowth upto 44% whereas, calcium channel blockers such as diltiazem or verapamil produce enlargement upto 20% and 4% respectively.

Drug substitutions for cyclosporine are more limited. The newer drug substitute tracolimus, is used in place of cyclosporine. There is some evidence that azithromycin decrease the severity of cyclosporine induced enlargement.

NON-SURGICAL APPROACHES: The primary aim of non-surgical approaches is to reduce the

inflammatory component in the gingival tissues and thereby avoid the need for surgery (Somacarrera et al. 1997).

Ideally preventative programmes should be instituted before the initiation of drug therapies implicated in DIGO (Modeer & Dahllof 1987).

ANTISEPTIC MOUTHWASHES Adjunctive chemical plaque removal has also been used in the

management of DIGO

Animal studies have shown that regular application of a chlorhexidine

solution to rats medicated with cyclosporin resulted in significantly less

overgrowth than in control animals (Pilatti & Sampaio 1997).

In humans chlorhexidine has, to date, only been evaluated in the

management of phenytoin- induced gingival overgrowth, when regular use

of this mouthwash helps to reduce the recurrence rate after surgery

(O’Neil & Figures 1982)

However, the unwanted effects of chlorhexidine of bacterial resistance and

taste disturbance limit its long-term use.

Systemic Antibiotics: Short courses of azithromycin and metronidazole have been evaluated in

the management of DIGO in organ transplant patients. However, the results of these studies are conflicting.

There is evidence to suggest that a combination of oral hygiene reinforcement and systemic antibiotics may be beneficial in the management of DIGO (Glaude & Snyder 1990).

Complete remission of cyclosporine induced gingival overgrowth has been reported in four renal transplant patients after a 7-day course of metronidazole (Wong et al. 1994)

Furthermore, in a larger study of 13 children, no improvement in overgrowth were seen at the end of a 3- month period (Aufricht et al. 1997).

Azithromycin has also been evaluated in the management of cyclosporine induced gingival overgrowth.There are two suggested mechanisms by which azithromycin may act in this context.

Firstly by reducing concomitant bacterial infection and hence inflammation (Mesa et al. 2003). or secondly by increasing the phagocytic activity of gingival fibroblasts, thereby reversing the ability of cyclosporin to decreases collagen degradation (Paiket al. 2004).

SURGICAL MANAGEMENT OF DIGO: If any drug substitution is attempted, it is important to allow for a

6- to 12 month period of elapse between discontinuation of offending drug and possible resolution of gingival enlargement before a decision to implement surgical treatment is made.

Scalpel Gingivectomy: The surgical treatment of choice is the gingivectomy, which was

first advocated for drug-induced gingival overgrowth in 1941 (Thompson & Gillespie 1941).

Gingivectomy has the advantage of simplicity and quickness but presents the disadvantages of more postoperative discomfort and increased chance of postoperative bleeding.

It also sacrifices keratinized tissue and does not allow for osseous recontouring .

The clinician’s decision between the two surgical techniques available must consider the extension of the area to be operated, the presence of periodontitis and osseous defects, and the location of the base of the pockets in relation to the mucogingival junction.

In general, small area (up to 6 teeth) of drug induced gingival enlargement with no evidence of attachment loss can be effectively treated with the gingivectomy technique.

An important consideration is the amount of keratinized tissue present, that at least 3mm in the apico-coronal direction should remain after the surgery is completed.

GINGIVECTOMY PROCEDURES: Gingivectomy means excision of the gingiva. Robicsek (1884) pioneered the so called procedure gingivectomy. Gingivectomy was later defined by Grant et al(1979) as being “the excision of soft tissue wall of a pathologic periodontal pocket”. The surgical procedure, which aimed at “pocket elimination”, was usually combined with recontouring of the diseased gingiva to restore physiologic form.

Gingivectomy is the excisional removal of gingival tissue for pocket reduction or eliminaton.

Gingivoplasty is the reshaping of the gingiva to attain a more physiologic contour; a contour that allows a gradual rise of tissue interproximally and fall on the labial & lingual surfaces.

INDICATIONS:

Elimination of suprabony pockets. Elimination of gingival enlargement. Elimination of suprabony periodontal abscesses. To eliminate soft tissue craters resulting from disease or

subsequent to other surgical procedures. To create clinical crown length for restorative or

endodontic purposes when ostectomy is not required.

CONTRAINDICATIONS: The need for bone surgery or examination of bone shape

and morphology. Situations in which the bottom of the pocket is apical to

the mucogingival junction. Esthetic considerations. Acute inflamed gingiva. Inadequate oral hygiene by the patient. Presence of large osseous ledges and exostoses. Inadequate depth of the vestibule. An increased caries rate that jeopardizes maintenance of

the dentition. When removal of the soft tissue would constitute an

unacceptable cosmetic compromise.

The gingivectomy procedure employed today was described in 1951 by Goldman.

STEP-1: The pockets on each surface are explored with a periodontal probe

and marked with a pocket marker. Each pocket is marked in several areas to outline its course on each

surface. Periodontal knives (eg. Kirkland Knives) are used for incisions on

the facial and lingual surfaces and those distal to the terminal tooth in the arch.

Orban periodontal knives are used for supplemental interdental incisions, if necessary and Bard-parker blade# 11 & 12 and scissors are used as auxillary instruments.

STEP-2 : The incision is started apical to the points marking the

course of the pockets and is directed coronally to a point between the base of the pockets and the crest of the bone.

It should be as close as possible to the bone without exposing it to remove the soft tissue coronal to the bone.

Discontinuous or continuous incisions are used.

The incision should be beveled at approximately 45 degrees to the tooth surface and should recreate, as far as possible, the normal festooned pattern of gingiva.

STEP-3: Remove the excised pocket wall, clean the area, and

closely examine the root surface. The most apical zone consists of a band like light zone where the tissues were attached, and coronally to it some calculus remnants, root caries, or root resorption may be found. Granulation tissue may be seen on the excised soft tissue.  

STEP-4: Carefully curette out the granulation tissue and remove

any remaining calculus and necrotic cementum, so as to leave a smooth and clean surface.  

STEP-5: Cover the area with surgical pack.

GINGIVECTOMY BY ELECTROSURGERY:Advantages: Permits adequate contouring of tissue and

controls hemorrhage.Disadvantages: Electrosurgery cannot be used in patients

who have noncompatible or poorly shielded cardiac pace makers.

The treatment causes an unpleasant odour. The heat generated can cause tissue damage

and loss of periodontal support when electrode is used close to bone.

Cannot be used in procedures that involve proximity to bone such as flap operations or for mucogingival surgery.

Technique: The removal of gingival enlargements and gingivoplasty is performed

with needle electrode, supplemented by the small ovoid loop or the diamond–shaped electrodes for festooning.

A blended cutting and coagulation (fully rectified) current is used. In all reshaping procedures, the electrode is activated and moved in a

concise shaving motion. For heamostasis, ball electrode is used. Hemorrhage must be controlled by direct pressure (via compression or

hemostat) first; then the surface is lightly touched by coagulation current. Electrosurgery is helpful for the controlling of isolated bleeding points. Bleeding areas located interproximally are reached with a thin, bar

shaped electrode.

The use of electrosurgery should be limited to superficial procedures such as removal of gingival enlargements, gingivoplasty, relocation of frenum and muscle attachments and incision of periodontal abscess and pericoronal flaps.

GINGIVECTOMY BY CHEMOSURGERY: Techniques to remove gingiva using chemicals such

as 5% formaldehyde or potassium hydroxide have been described in the past but not currently used.

Disadvantages: The depth of action cannot be controlled, and

therefore healthy connective tissue underlying pocket may be injured.

Gingival remodeling cannot be accomplished effectively.

Epithelialization and re-formation of junctional epithelium and re-establishment of the alveolar crest fiber system occur more slowly in chemically treated gingival wounds than in those produced by scalpel.

Laser Gingivectomy:

The dental laser may be another useful alternative treatment to

conventional gingivectomy techniques.

The use of laser surgery to remove excess gingival tissue has been

described by a number of authors (Barak & Kaplan 1988, Gold

1991, Hattler et al. 1992, Roed-Petersen1993)

Lasers have remarkable cutting ability and they also generate a

coagulated tissue layer along the wall of the laser incision which

promotes healing (Goharkhay et al. 1999)

Other advantages of the use of laser in correcting DIGO include a relative bloodless operative and post-operative field, greater accuracy in making incisions, sterilization of the operating field, minimal swelling and scarring, vaporization and cutting with much less post-operative pain (Barak & Kaplan 1988, Roed- Petersen 1993, Mavrogiannis et al.2004).

Comparison of laser to scalpel excision in the management of DIGO using a split-mouth crossover design study demonstrated a significantly lower rate of recurrence for laser gingivectomy over a 6-month follow-up period (Mavrogiannis et al. 2006).

The study employed the diode laser at a wavelength of 810 nm. Post-operative pain scores were similar for the two treatments. The laser gingivectomy was also preferred by the patients.

In a comparative study scalpel, electrosurgery,and CO2 laser were evaluated for mucosal incisions and excisions (Liboon et al. 1997).

The scalpel was quicker to use for both incision and excision, followed by electrosurgery and the CO2 laser. There is also a significant cost element to be considered in addition to the advantage of the scalpel over other techniques.

Wound Healing after gingivectomy: The initial healing events after the procedure are

directed towards establishing hemostasis and the production of a fibrin clot to cover the wound surface.

This initial lag phase is followed by cellular proliferation of epithelium at the wound margins as demonstrated by increased DNA synthesis ( 12-24 hrs).

Proliferation of vascular tissues, which peaks at 3-4 days after surgery.

35-48 hrs: the epithelial cells resulting from the cellular replication begin to migrate across the cut connective tissue under the fibrin clot to cover the wound.

These cells migrate at a rate of approximtely 0.5 mm per day until the wound surface is covered.

Depending on the extent of wound surface, it may take 1-2 weeks to complete surface epithelialization.

The source of these migrating cells is from wound margin and the residual epithelial cells that were not totally eliminated by external bevel incision.

The epithelial growth proceeds until it contacts the root surface and a new junctional epithelial attachment is established.

The subsequent proliferation of connective tissue adjacent to the root results in the formation of a new gingival sulcus.

By approximately 14 days the tissue assume a normal clinical form, although some hypervascularity may persist.

Remodelling of the tissues as evidenced by changes in color, may continue for a period of 3 months.

FLAP TECHNIQUE FOR GINGIVAL ENLARGEMENT: Larger areas of gingival enlargement ( more than 6 teeth) or areas

where attachment loss and osseous defect are present should be treated by the flap technique, as should any situation in which the gingivectomy may create a mucogingival problem.

The periodontal flap technique used for the treatment of gingival enlargement is a simple variation of the one used to treat periodontitis, basic steps in the technique are described as follows.

1. After anesthetizing the area, sounding of the underlying alveolar bone is performed with a periodontal probe to determine the presence and extent of osseous defects.

2. With a # 15 Bard-Parker blade, the initial scalloped internal bevel incision is made at least 3mm coronal to the mucogingival junction, including the creation of new interdental papillae.

3. The same blade is used to thin the gingival tissues in a buccolingual direction to the mucogingival junction.

3. Using an orban knife, the base of the each papilla connecting the facial and lingual incisions is incised.

4. The excised marginal and interdental tissues are removed with currete.

5. Tissue tabs are removed , the roots are thoroughly scaled and planed and bone is recontoured as needed.

7.The flap is replaced and if necessary trimmed to reach the bone tooth junction exactly. The flap is then sutured with an interrupted or a continuous matteres technique and the area is covered with a periodontal dressing.

Another situation in which the periodontal flap proves to be useful in DIGO is in assisting tooth eruption in younger patients.

Maintainance: Meticulous home care[Nishikawa S, Tada H 1991] ,CHX mouth

rinses[Saravia 1990] and professional cleaning can decrease the rate and the degree at which recurrence occurs.

CANNABIS: Excessive use of marijuana has been associated with gingival

enlargement. This resembles other forms of DIGO and may be accompanied by gingivitis and alveolar bone loss.

PUBERTY: Young women begin producing sex hormones ,

estrogen and progesterone. These hormones influence the periodontium and influence the physiology of host-parasite interactions in the oral cavity. Hormones may increase the permeability of blood vessels of the periodontium and micro organisms may react to the increased availability of hormones in the oral fluids. Thus , the gingiva demonstrates a more exaggerated response to microorganisms.

The incidence and severity of gingivitis increases at puberty. Gingivitis eases in later stages of puberty, usually without substantial treatment.

Dental strategies for adolescent women: Gingivitis response well to scaling, root planing

and anti microbial rinsing and good plaque removal practices. Compromised or otherwise susceptible individuals may require further periodontal care.

PREGNANCY: Contrary to the myth that “ a tooth is lost for every

pregnancy”, there is no evidence that calcium is withdrawn from maternal dentition in any significant amount. Gingivitis is the most prevalent oral manifestation associated with pregnancy.

It is present in 30-100% of pregnant women. The hormonal and vascular changes of pregnancy cause an exaggerated response to local irritants.

Another gingival change that may occur is single, tumor like growth on the interdental papillae referred to as pregnancy tumor. The histologic appearance is similar to pyogenic granuloma. Reported frequency ranges from 0-9.6%.

The lesion occurs most frequently on the labial aspect of the maxillary anterior region during the second trimester, grows rapidly, but seldom becomes large than 2cm in diameter. This growth is also an exaggerated response to local irritants.

Surgical excision is often required after the pregnancy.

Plaque control during pregnancy: good plaque control is important for pregnant pt because of exaggerated inflammatory response during pregnancy. Scaling and root planing can be done any time during pregnancy.

Treatment during pregnancy: Elective treatment should be avoided in the first

trimester and the last half of third trimester. The second trimester is the safest period for treatment and the focus should be on active disease and eliminating potential problems that occur later in the pregnancy. Radiation should be avoided if possible.

Enlargements in vitamin C deficiency: Severe vitamin C deficiency has been one of the

earliest nutritional deficiency to be examined in the oral cavity.[Lind 1953]

It is essentially due to conditioned response to bacterial plaque

Acute vitamin deficiency does not by itself cause gingival inflammation but cause hemorrhage, collagen degeneration and edema of the gingival connective tissue.

The combined effect of acute vitamin deficiency and inflammation produces massive gingival enlargement.

Correction of the deficiency and treatment of local factors regresses the enlargement.

Plasma cell gingivitis: Also referred to as Atypical gingivitis and plasma cell

gingivo stomatitis and often consists of mild marginal enlargement extending upto the attached gingiva.

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

It is thought to be due to allergic in origin possibly related to components of chewing gum, dentifrices, or various diet components.

Treatment include•Cessation of exposure to the allergen brings resolution of the lesion •Professional oral hygiene measures.

PYOGENIC GRANULOMA: Is a common benign gingival mass that

occasionally can present on other intraoral sites such as buccal mucosa or the tongue. It appears as soft, smooth-surfaced, bright red raised tissue that has tendency to bleed.

The lesions may be caused by irritants such as calculus or denture irritation or as a result of certain hormonal changes. Because of irritation ,the fibrovascular connective tissue becomes hyperplastic and the proliferation of granulation tissue gives rise to the observed lesion( Silverman 2002).

A recent case report has described formation of a pyogenic granuloma as a result of injury to primary tooth( Aguilo 2002).

It usually appears as red, blue or purple gingival masses, broad based or pedunculated. They may become ulcerated.

Occasionally nonspecific granulation tissue may proliferate from a recent extraction socket and resemble a pyogenic granuloma. Such a lesion called as “ epulis granulomatosum”.

Removal of the irritants and surgical excision of the lesion and involved connective tissue is the treatment of choice( Akyol 2001).

Pyogenic granuloma is highly vascularized, and in a case report an Nd: YAG laser excision was used because of its superior coagulation properties( Powell 1994). Oral hygiene and the use of soft tooth brushes during pregnancy is important in preventing these pyogenic granuloma( Wang 1997).

LEUKEMIA: Leukemia is a serious maligant disease characterized

by the neoplastic proliferation of the leucocyte precursor cells within the haemopoetic tissues such that there is usually marked increase in circulating white blood cells and infiltration of these cells into tissues, particularly the lymph nodes.

Several factors are implicated in the aetiology of leukaemia namely, radiation, chemical injury, genetic factors, immune deficiency and viral infectons.

Gingival enlargement, which is usually generalized and variable in its severity, was apparent in 36% of the individuals with acute forms of leukemia.( Lynch & Ship 1967). Gingival swelling due to actual infiltration by leukemic cells is relatively uncommon.

This swelling is considered to be a consequence of plaque-induced chronic inflammation. Gingival tissues are considered more susceptible to leukemic cell infiltration due to its microanatomy and the constitutive expression of endothelial adhesion molecules, which enhance leukocyte infiltration.

In children the changes are most commonly observed around the last developing molar tooth(Curtis 1971) and involve the periapical part of the periodontium than the crestal part.

The relative frequency of gingival changes, including hyperplasia, haemorrhage and ulcerative necrosis are considered a consequence of the high incidence of chronic gingivitis. Several authors emphasized that the gingival changes are less marked or even suppressed if excellent oral hygiene measures are maintained.( Sinrod 1957, Carranza 1979).

The hematologist should be consulted before periodontal treatment is instituted.

Administer antibiotic coverage before any periodontal treatment because infection is a major concern.

During acute phases of leukemia, patients should receive only emergency periodontal care. Any source of potential infection must be eliminated to prevent systemic dissemination. [Fischman S 1983]

After acute symptoms subside attention is directed to correction of gingival enlargement.

The rationale is to remove the local irritating factors to control the inflammatory component of the enlargement.

The enlargement is treated by scaling and root planing carried out in stages.

The initial treatment consists of gently removing all loose accumulations with cotton pellets, superficial scaling and instruct the patient in oral hygiene for plaque control.

It should include chlorhexidine mouthwashes. Progressively deeper scaling is carried out at

subsequent visits. Treatment is confined to small area of the mouth to

facilitate control of bleeding. Antibiotics are administered systemically the evening

before and 48 hours after each treatment to reduce the risk of infection.

PRELEUKEMIA: Is a syndrome of haemotological abnormalities

that often proceeds to leukemia. This condition may last for 6-24 months before leukemia develops. The gingivae were hyperplastic, oedematous and haemorrhagic.

SARCOIDOSIS: Sarcoidosis is relatively common, multisystem

disease of unknown etiology. A number of studies suggest that both host and environmental factors are importatant in the development of the disease. although unique environmental factors or infectious agents have yet to be identified, a number of studies have identified spatial , seasonal, and occupational clustering of sarcoidosis cases. ( Thomas 2003)

Moreover, there is ample data to suggest that sarcoidosis is a Th 1 disorder, thus supporting a role for external agent in the development of the disease.

Clinical findings: Pulmonary involvement is characteristic of the

disease, with most symptomatic patients presenting with a persistent dry cough, dyspnea or chest pain. Oral involvement in sarcoidosis is rare. Although in some patients the oral lesions may be the initial manifestations of the disease.

Most lesions present as painless, submucosal nodular or multinodular growths or swellings. Sarcoidosis of gingiva typically presents as a diffuse enlargement.

Involvement of the jawbones has also been reported, with the most charcteristic presentation being that if an ill-defined .Radiolucency involving tooth bearing region. In cases, the patient may present with progessive bone loss and increasing mobility of the adjacent teeth, thus mimicking periodontal disease.

Treatment and prognosis: The decision to treat a patient with sarcoidosis

should be based upon the extent of the disease and the organs and tissues involved, the stability of the disease over a period of continued observation, and the likelihood of therapeutic.

Patients with only mild symptoms or stable disease often donot require any treatmant. A relatively brief course of low- dose systemic corticosteriods, ranging from weeks to months, often is prescribed for patients with more severe or progressive disease. Despite therapy these patients typically have a worse overall prognosis.

WEGENER’S GRANULOMATOSIS: Rare disease characterized by acute

granulomatous necrotizing lesions of the respiratory tract.

The granulomatous papillary enlargement is reddish purple and bleeds easily on stimulation.

The use of immunosupressive drugs has produced prolonged remissions in more than 90% of patients.[Skach M 1970]

Treatment of a neoplastic conditions : Benign tumors of gingiva: 1. Fibroma 2. Papilloma 3. Peripheral giant cell granuloma 4. Gingival cyst Malignant tumors 1. Squamous cell Carcinoma 2. Malignant melanoma 3. Sarcoma

Papilloma: Benign proliferations of surface epithelium

associated with the Human Papilloma Virus. Appear as solitary wart-like or cauliflower like

protuberances. May be small and discrete or broad, hard elevations

with minutely irregular surfaces.  

Treatment: Consists of surgical excision including the base of

this mucosa into which the pedicle or stalk inserts. Removal should never be accomplished through the

pedicle. If the tumor is properly excised recurrence is rare.  

Fibroma: Arise from the gingival connective tissue or from

PDL. Slow growing spherical tumors . Tend to be firm or nodular and usually pedunculated.

Treatment: Conservative surgical excision .

Central giant cell granuloma: Arise within the jaws and produce central cavitations. Occasionally create a deformity of the jaw that

makes the gingiva appear enlarged.

PERIPHERAL GAINT CELL GRANULOMA: Is a benign reactive gingival lesion(Flaitz 2000).

This uncommon lesion occurs as a reparative response of the connective tissue to gingival irritants. The biologic origin of the lesion is thought to be periodontal ligament or the periosteum ( Regezi 2003).

Poor oral hygiene is thought to be a predisposing factor(Bhat 1999).

The lesion appears as a broad based blue/red mass. The most common location is the gingival tissue between the first molar and the incisors( Regezi 2003).

Surgical excision along with the elimination of irritating agent is the treatment of choice(Flaitz 2000).

Treatment include Curettage or surgical excision. The lesions so treated fill in with new bone and heal

with no difficulty.

Gingival cyst: Appear as localized enlargements that may involve

the marginal and the attached gingiva.Treatment: Local surgical excision is recommended . Removal is followed by uneventful recovery . Lesions do not tend to recur.

Squamous cell Carcinoma: Most common malignant tumor of the gingiva. It may be exophytic, presents as a irregular outgrowth

or ulcerative which appears as a flat erosive lesion. It is often symptom free, sometimes it becomes

evident after tooth extraction. They are locally invasive involving the underlying

bone and PDL of adjoining teeth and adjacent mucosa.

Treatment: Radiation and surgical removal is done. But the disadvantages being radiation hazards and

the location of this lesion is a surgical problem. Prognosis is very poor.

Malignant melanoma: Tends to occur in hard palate and maxillary gingiva of

the old persons. It is darkly pigmented and often preceded by the

occurrence of localized pigmentation.

Treatment: Surgical excision. Regional lymph node dissection is indicated when

nodes are involved. Chemotherapy, immunotherapy and radiation

therapy have been used in the treatment.

Sarcoma: Fibrosarcoma, lymphosarcoma, reticulum cell

carcinoma of the gingiva are rare. Kaposi sarcoma often occurs in patients with AIDS-

particularly affecting the palate and gingiva.

Treatment: Antiretroviral agents. Laser excision. Radiation therapy or Intralesional injection with

vinblastine(0.1mg). Interferon alpha.

False enlargements: These are not true enlargements but may appear as

such a result of increase in size of underlying osseous or dental tissues.

The gingiva presents with no abnormal clinical features except the massive increase in the size of the gingiva.

 

Underlying osseous lesions:Enlargement of the bone adjacent to the gingival area

occurs most commonly in Tori and Exostoses, but also occurs in Paget’s disease Fibrous dysplasia Cherubism Ameloblastoma Osteoma and Osteosarcoma.

TORI AND EXOSTOSES:GENERAL DISCRIPTION ANDCLINICAL PRESENTATION:

Exostoses are benign bony overgrowths of the facial bones, usually the maxilla and mandible. Most commonly, exostoses occur singly on midline of palate, where they are reffered to as palatal tori.exostoses known as mandible tori cn also be found on lingual surface of mandible; those tha multiply on facial surfaces of the maxilla and mandible are known as multiple exostoses. Tori and exostoses are covered by epithelium and are frequently asymptomatic.

TREATMANT OPTIONS: Because exostoses are benign processes, no treatment is indicated.

Exceptions are situations when the exostoses interfere with a planned removable appliance and the rare instances when speaking and eating are compromised.occasionally exostosis removal is warranted when the overlying mucosa is repeatedly traumatized.

Paget’s disease: Treatment: No specific treatment. Vitamin, hormone and radiation therapy has

been tried with sporadic reports of cure. Promising result obtained with calcitonin and parathromone antagonist produced by the thyroid gland, which suppresses the bone resorption.

Cherubism: Treatment: Cherubism although progressing rapidly during early childhood

regresses as the patient approaches puberty.When the patient becomes older past puberty, surgical correction of the jaws some times advised.

Fibrous dysplasia: Mild forms can be treated surgically . Severe forms are impossible to treat because they tend to be progressive.

For this reason x-ray radiation has been used with some success.

Ameloblastoma: Treatment: Radical and conservative surgical excision Curettage and chemical electrocautery Radiation therapy or Surgery and radiation

Underlying dental tissues: During the 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 is called as developmental enlargement.

when complicated by marginal inflammation, the composite picture gives the impression of extensive enlargement

Treatment to alleviate the marginal inflammation, rather than resection of the enlargement is sufficient.

GINGIVAL FIBROMATOSIS: Hereditary gingival fibromatosis(HGF) is a non

inflammatory enlargement of the attached gingival-fibrous tissue.( Noyan U 1994). It is often isolated condition, but it also has been in some hereditary conditions such as cherubism, Prune-belly syndrome.

Increased extracellular matrix synthesis such as collagen I and fibrinectin and increased fibroblast proliferation have been thought to contribute to the condition( Coletta 1998).

In a recent case report it was suggested that HGF might result from an increased biosynthesis of collagen and glycosaminoglycans rather than from cell proliferation( Saygun 2003).

HGF may appear as single or multiple firm, fibrous tissue masses the same color or lighter than the surrounding tissues.

The treatment is complete excision by conventional surgery or laser surgery.( Brown RS 1995).

LABAND SYNDROME: Is a rare disorder characterized by a broad spectrum of lesions. Etiology- genetic.Clinical features: Gingival fibromatosis is a constant feature and is manifested at birth

or within the first 2 months of life. The gingiva are characteristically enlarged and cover the crowns of

teeth. Usually lobulated and slightly firm on palpation. Macroglossia and enlargement of lips are less common

manifestations. Hepatomegaly,splenomegaly and learning disability have been noted.

Treatment:oGood oral hygeine.oGingivectomy.

FAMILIAL ACANTHOSIS NIGRICANS: Is an uncommon benign mucocutaneous disorder,

characterized by papillary lesions and occasional skin discolouration.

Etilogy- genetic. Clinical features: Gingival enlargement and in particular interdental

papillae may be present. The oral mucosal lesions appear as multiple,

small, painless papillomatous growths. The disorder usually develops during childhood or

at puberty.

Treatment:oGingivectomy and good oral hygeine for gingival lesions.oSurgical reconstruction of skin lesion in case of severe aesthetic problems.

STURGE-WEBER ANGIOMATOSIS: Typically unilateral heamangiomas, usually

capillary, on the attached gingiva and the alveolar mucosa may be seen occasionally leading to gingival hyperplasia.

Appears red or purple in colour.Treatment: Laser therapy is recommended.

KLIPPEL-TRENAUNAY-WEBER SYNDROME: Is an uncommon dysplastic vascular disorder. Etiology-dysplastic malformation. The gingival lesions appear as capillary or

cavernous haemangiomas occasionally leading to gingival overgrowth that may cover the crown of the teeth

Premature tooth eruption and alveolar bone overgrowth may occur.

Treatment: Laser treatment may improve skin lesions.

HURLER’S SYNDROME: Is a rare and the most common & severe form, in

the group of mucopolysaccharide metabolic disorders.

Etiology-genetic. - defect of enzyme alpha-L-iduronidase

resulting in accumulation and deposition of heparin sulphate and dermatan sulphate within the tissue.

Gingival overgrowth particularly in the anterior region of maxilla.

The overgrowth due to mouth breathing association with dental plaque and deposition of heparin & dermatan sulphate within gingiva.

Disease presents during infancy and often leads to death usually before 10 yrs of age.

Treatment:oGood oral hygeine.oGingivectomy.

DENTURE-INDUCED FIBROUS HYPERPLASIA:( epulis fissuratum, inflammatory hyperplasia,

denture hyperplasia of oral mucosa.) Is a connective tissue lesion that appears as a

fibrous growth under and around the border of ill-fitting dentures. Ill-fitting dentures can cause trauma to the underlying tissue.

Chronic trauma over a long period of time can cause a reparative response, which results in fibrous tissue hyperplasia. It is mostly asymptomatic.

If the denture is removed for a long period of time or relined, the underlying fibrous tissue may reduce in size. Any remaining tissue can be removed by surgical excision. Construction of new denture prevents the recurrence.

CROHN’S DISEASE: Crohn’s disease is a chronic granulomatous

disorder that may involve any portion of the gastrointestinal teact, including the oral cavity. Environmental and genetic factors seem to play a role in pathogenesis of crohn’s disese, but the extract etiology remains unknown.

The classical presentation is that of a patient complaining of various constitutional signs and symptoms, abdominal pain, and repeated bouts of diarrhea.

Oral lesions are indentified in upto 60% of patients and may be the initial manifestation of disease in 5 to 10% of affected individuals.

Gingival lesions, usually in the form of generalized edema, arythema, and hyperplasia, are common. In most cases the attached gingiva is involved, usually in the anterior facial region.

Treatment and prognosis: If the disease is restricted to the oral cavity. High-

potency topical or intralesional steroids may be sufficient.

RECURRENCE OF GINGIVAL ENLARGEMENT: Recurrence is the most common problem after

treatment in the management of gingival enlargement.

Residual local irritation and systemic or hereditary conditions causing non-inflammatory gingival hyperplasia are the responsible factors.

If the recurrence of chronic inflammatory enlargement occurs immediately after treatment indicates that all irritants have not been removed.

Food impaction and overhanging margins of restorations are the local conditions, which are commonly overlooked.

If the recurrence occurs after the healing is completed and normal contour is attained, that indicates inadequate plaque control by the patient.

If the recurrence occurs during the healing period as red, bead like, granulomatous masses that bleed on slight provocation indicates the proliferative vascular inflammatory response to local irritation, usually fragment of calculus on the root.

The condition is corrected by removal of granulation tissue, scaling and root planing.