Treatment of gingival enlargement - by Dr Harshavardhan Patwal

TREATMENT OF GINGIVAL
ENLARGMENT
Presented 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 ALLERGY
Clindamycin
•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:
AnticonvulsantsAnticonvulsants
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% formaldehydeor 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.

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.

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