Periodontal Diseases

Periodontium
• The periodontium (peri - around, odonto - tooth) includes the following tissues:
1. Gingiva
2. Periodontal ligament
3. Root cementum
4. Alveolar bone
•The main function of periodontium is to attach the tooth to jaw bone and to
maintain the integrity of the masticatory system
Deposits on teeth
• The organic coverings of tooth enamel are divided into two types:
1. Anatomic structures
2. Acquired pellicle
• The anatomical covering , formed during the developmental and eruptive stages, is
known as Nasmyth’s membrane or enamel cuticle, with its remnants persisting
throughout tooth’s life.
• Deposits on teeth include –
a) Pellicle
b) Dental stains
I. Intrinsic Stains
II. Extrinsic Stains
c) Calculus
Pellicle
• The acquired pellicle is a thin deposit formed shortly after eruption on the exposed
surface of the tooth.
• It is usually invisible and free of bacteria covering complete surface of the tooth.
• It is reformed within 30 mins of polishing and reaches its mature thickness of 0.1 to
0.8 microns within 24hrs.
• It is brownish stained, smooth and structure less deposit due to presence of tannins.
• Electron histochemistry indicates that pellicles are of salivary origin.
• It comprises of mucoproteins or glycoproteins similar to those in saliva.
• A persistent extraneous calcification was observed always in pellicle from the lingual
surfaces of the anterior teeth.
Dental Stains
• Pigmented deposits on the tooth surface are called Dental Stains or Extrinsic Stains.
• The stains that are incorporated into the tooth structure are known as Intrinsic Stains
and are seen in
1. Porphyria
2. Erythroblastosis fetalis
3. Tetracycline therapy
• Commonly seen stains are namely
I. Stains from Smoking
II. Brown Stains
III. Black Stains
IV. Green Stains
V. Orange Stains
Stains From Smoking:

• Due to collection of tobacco tars and

resins, a yellowish brown to black deposits
are formed on the tooth surfaces of the
people who often smoke.
• These stains vary from a light brown,
powdery deposit in occasional smokers to a
dense black tarry deposit in heavy
smokers.
• This is harmless to teeth although it should
be removed because of its objectionable
appearance and may act as nidus for
calculus or have irritating affect on gingiva.
• Staining may be severe in attrited tooth if
dentin is exposed.
Brown Stains:

• These are thin, brown, delicate, pellicle-

like structures that occur on teeth.
• They are thought to composed of salivary
mucin due to its occurrence on the
surfaces of the teeth that are closely
adjacent to orifices of salivary gland ducts.
• A delicate pigmented dental plaque called
mecentric line was described by Pickerill
as
- A plaque of brown or black dots that
coalesce to form a thin dark line on
enamel at the cervical margin of the
tooth which indicate relative freedom
from dental caries.
Black Stains:

• A thin black deposits on teeth which

are usually in narrow line or band, just
above the free gingiva.
• They are seen both in children and
adults.
• These are not associated with smoking
and may be caused by chromogenic
micro organisms.
• Micro flora of black stain is dominated
by actinomyces species.
• Black stains on primary teeth are
associated with dental caries.
Green Stains:

• They are usually heavy grey-green

stains especially prominent on gingival
third of maxillary anterior teeth.
• These are mostly seen in children.
• They appear to be soft or furry and
are difficult to remove suggesting
their association with the enamel
cuticle (Nasmyth’s membrane).
• Coloration of remnants of dental
cuticle, possibly by blood pigments
may be responsible for these stains.
Orange Stains:

• Occasionally a light thin deposit

of material of brick red or orange
color is seen on teeth.
• Cause of these stains is unknown
but believed to be due to
pigment producing micro
organisms.
• These can be easily removed and
are of no apparent significances.
• They may or may not recur.
 Classification of Periodontal Disease
Plaque Induced gingival disease
Gingival Diseases
Non Plaque Induced gingival lesions
Localized
Chronic Periodontitis
Generalized

Localized
Aggressive Periodontitis
Generalized

Necrotizing Periodontal Necrotizing Ulcerative Gingivitis (NUG)

Disease Necrotizing Ulcerative Periodontitis (NUP)
 Classification of Periodontal Disease
Gingival Abscess
Abscesses of Periodontium Periodontal Abscess
Pericoronal Abscess

Periodontitis as a manifestation of systemic disease

Endodontic-periodontal lesion
Periodontitis associated Periodontal-endodontic lesion
with endodontic lesions
Combined lesion
 Classification of Periodontal Disease
Localized tooth-related factors that
predispose to plaque-induced gingival
diseases or periodontitis
Developmental or
acquired deformities and Mucogingival deformities and conditions
conditions around teeth
Mucogingival deformities and conditions
on edentulous ridges

Occlusal trauma
Gingival Diseases
Gingival diseases are broadly classified into
I. Dental plaque-induced gingival diseases
II. Non plaque-induced gingival lesions
Plaque- induced Gingival Disease
• It is the most common form of gingival disease.
• It occurs on periodontium with no attachment loss or with a
previous attachment loss that is stable and not progressive.
• It is a result of interaction of plaque bacteria and defense cells of
host.
• This interaction is modified by local and systemic factors.
 Local factors
1. Microorganisms
2. Calculus
3. Food impaction
4. Faulty or irritating dental
restorations or appliances
5. Mouth breathing
6. Tooth malposition
Systemic factors
1. Nutritional deficiencies
2. Drug action
3. Endocrine changes associated with
puberty, pregnancy, menstrual
cycle, and diabetes
4. Allergy
5. Heredity
6. Psychic phenomena
7. Neutrophil dysfunction
8. Immunopathies
Clinical features

• Acute is a painful uncommon lesion with sudden onset and shorter duration.
• It may be localized or generalized, without underlying attachment loss.
• It sometimes involves only marginal gingiva known as marginal gingivitis.
• Hyperaemia and swelling are localized area, termed as traumatic crescent.
• Diffuse gingivitis affects marginal gingiva, attached gingiva and interdental gingiva
• Color of free or marginal gingiva changes from light or dark pink to red or reddish blue,
as hyperaemia and inflammatory infiltrate become more intense.
• Oedema and loss of stippling are evident.
• When enlargement is increased, due to oedema and fibrosis because of chronic
inflammation, it is called chronic hyperplastic gingivitis.
• Suppuration of gingiva is seen in advanced chronic gingivitis.
Radiographic features
• There is no manifestation of changes in underlying bone.
• If bony changes are evident then it is periodontitis.

Histological features
• In chronic gingivitis, connective tissue is Infiltrated by lymphocytes, monocytes and
plasma cells.
• PMNLs are occasionally noted, beneath crevicular epithelium.
• This epithelium is usually non-keratinized, irregular and frequently ulcerated.
• The connective tissue has engorged capillaries in increased number, hyperaemia,
oedema and haemorrhage.
• There is a collection of polymorph nuclear leukocytes and lymphocytes at the junction
of epithelial attachment to the tooth.
• Glycogen content of granular and spinous layers increases.
• Mast cells containing granules of sulphonated mucopolysaccharide; and also the activity
of alkaline phosphatase increases in inflamed gingiva.
Treatment and Prognosis
• The irritants are removed ,then the inflammation with swelling due to
oedema, hyperaemia and leukocytic infiltration will disappear within hours
to few days.
• Proper brushing of teeth and frequent prophylaxis is required.
• Mechanical removal of plaque.
• Chemical plaque control measures such as using mouthwash containing
chlorhexidine, listerine or triclosan.
 Non-Plaque Induced Gingival Diseases
Gingival diseases of specific bacterial origin
Non Plaque Induced

Gingival diseases of viral origin

Gingival Diseases

Gingival diseases of fungal origin

Gingival diseases of genetic origin
Gingival manifestations of systemic conditions
Traumatic lesions
Foreign body reactions
Not otherwise specified
Necrotizing Gingivostomatitis
• Necrotizing ulcerative gingivitis, necrotizing ulcerative periodontitis and necrotizing
stomatitis are together termed as Necrotizing gingivostomatitis.
• The predisposing factors may include emotional stress, immunosuppression, HIV
infection, smoking, malnutrition and preexisting gingivitis.

Necrotizing Ulcerative Gingivitis

(Vincent infection, Trench mouth, Acute Ulceromembranous Gingivitis, Fusospirochetal
Gingivitis, Acute Ulcerative Gingivitis)
• It manifests both acute and recurrent (susacute) phases.
• It involves primarily the free gingival margin, crest of gingiva and interdental papillae.
• It is termed Vincent angina, when lesions spread to soft palate and tonsillar areas.
• Diagnostic triad: Pain
Interdental ulceration
Gingival bleeding
• It is termed as Necrotizing ulcerative periodontitis when bone loss occurs, with
attachment loss.
Epidemiology
• It is apparent during world war I, among the troops in trenches hence termed trench mouth.
• It is more common among young and middle aged adults.

Aetiology
• It is believed to be caused by Fusiform bacillus and Borreliavincentii – a spirochete.
• Bacteriodes melaninogenicus and Bacteriodes intermedius are also confirmed to be
causative agent of necrotizing ulcerative gingivitis.
• Increase in IgG and IgM antibody titers to spirochetes and increased IgG titers to B.
melaninogenicus are found through ELISA and indirect immunofluorescence.

Predisposing factors
• Psychological stress is important factor.
• Other factors include immunosuppression (HIV infected), smoking, upper respiratory tract
infection, local trauma, poor nutritional status and poor oral hygiene.
• Also decrease in resistance to infections and deficiency in various vitamins may also act as
predisposing factors.
Clinical features
• Characterized by the development of painful, hyperaemic gingiva and sharply
punched-out, crater like erosions of sudden onset.
• The ulcerated papillae and free gingiva bleeds on touch and a fetid
unpleasant odour.
• The gingiva become covered with a greyish-green necrotic pseudomembrane.
• Inability to eat due to severe pain (superficial pressure type) and tendency
for bleeding.
• Headache, malaise and low-grade fever may be seen.
• Excessive salivation with metallic taste and regional lymphadenopathy are
usually present.
• Incubation zone : areas where debris and microorganisms retain, where
recurrence begins.
Necrotizing Ulcerative Gingivitis
Histological features
• It reveals an acute gingivitis with extensive
necrosis.
• Surface epithelium-ulcerated and replaced by a
thick fibrinous exudate, or pseudomembrane,
containing many PMNLs and microorganisms.
• Lack of keratinization is a common feature.
• Connective tissue- infiltrated by PMNLs and
shows intense hyperaemia.
• Vast no. of both spirochetes and fusiform bacilli
are found on surface of living tissue beneath
necrotic pseudomembrane.
• Spirochetes are also found between viable
epithelial cells.
Treatment and Prognosis
• Superficial cleansing of oral cavity with chlorhexidine, diluted hydrogen
peroxide or warm saltwater in early acute stage.
• Followed by scaling and polishing , coupled with antibiotics sometimes.
• Topical anesthetics to reduce pain.
• Recontouring of gingival papillae when there’s considerable destruction
by- round toothpicks or gingivoplasty.
• Occasionally end up as gangrenous stomatitis or Noma, septicemia,
toxemia and even death.
Desquamative Gingivitis
• It is not a specific disease entity but rather a clinical manifestation of several
diseases.
• Specific degenerative disease of gingival tissues, called as gingivosis.
• Intense redness and desquamation of surface epithelium is seen.

Aetiology
• Suggestive causative factors are
1. Certain dermatoses
2. Hormonal influences
3. Abnormal responses to irritation
4. Chronic infections
5. Idiopathic
• Dermatoses are numerically the most important of the causative factors.
• The most important dermatoses presenting these oral findings are
I. Cicatricial pemphigoid(benign mucous membrane pemphigoid)
II. Pemphigus
III. Lichen planus
• Other diseases such as pemphigus vulgaris, epidermolysis bullosa, systemic lupus
erythematosus and linear IgA disease may also present Desquamative gingivitis.
Pericoronitis
• It is an inflammatory lesion
occurring around the impacted
or partially erupted tooth.
• Incomplete eruption provides a
large stagnation area for food
debris under the gingival flap.
• It becomes infected resulting in
chronic inflammation of
pericoronal flap.
• If debris and bacteria are deeply
entrapped, an abscess may form
called Pericoronal Abscess.
Clinical features
• Mandibular 3rd molar – commonly involved tooth.
• Pain and swelling of pericoronal tissue around affected tooth.
• Difficulty in chewing and opening of mouth.
• Also fever, malaise and regional lymphadenopathy may be seen.

Histological features
• Epithelium of pericoronal flap shows - hyperplasia
Intercellular oedema
Leukocytic infiltration.
• Connective tissue – increased vascularity, dense diffused infiltration
with lymphocytes, plasma cells and PMNLs.
Management
• Entrapped food debris must be removed.
• Malposed teeth should be ground or extracted.
• If the tooth is in favorable position, surgical removal of pericoronal
flap (Operculectomy) is advocated.
• Administrative of antibiotics to relieve the symptoms and to prevent
the spread of infection to adjacent tissue spaces.
Gingival Enlargement

• The enlargement of gingiva may be localized to one papilla or may

involve many or all gingival papillae throughout mouth.
• It is usually prominent on labial and buccal surfaces, occasionally
lingual gingiva but doesn’t involve the vestibular mucosa.
• Gingival enlargements can be classified based on aetiological factors
and pathological changes as follows:
 1. Inflammatory gingival enlargement
Gingival Enlargement
2. Drug – induced gingival enlargement
3. Enlargement associated with systemic factors
a. Conditioned enlargement
b. Enlargements due to systemic factors
4. Idiopathic gingival enlargement
5. Neoplastic enlargement
6. False enlargement
1. Inflammatory Gingival
Enlargement
• It results from prolonged chronic inflammation
of gingival tissue because of local irritants such
as poor oral hygiene, accumulation of dental
calculus or mouth breathing.
• In this, the gingivae are soft, oedematous,
hyperaemic or erythematous and sensitive to
touch.
• Bleed easily and presents with glossy, non
stippled surface.
• The local irritation results in hyperaemia,
oedema and lymphocytic infiltration.
• Also cause proliferation of fibrous connective
tissue.
2. Drug- induced Gingival Enlargement
• Caused due to use of anticonvulsants, immune suppressants and calcium channel
blockers.
• Anticonvulsants - Diphenylhydantoin (dilantin sodium) Was first anticonvulsant
reported to cause gingival enlargement.
• Other hydantoins responsible are ethotoin and mepheytoin
• Valproic acid, methosuximide and succinimides may also be responsible.
• Dilantin sodium induces enlargement in 50% of patients.
• Phenytoin stimulates proliferation of fibroblast-like cell in tissue culture and decreases
the collagen degradation.
• Cyclosporine, a potent immunosuppressive agent is responsible in 30% of patients.
• Calcium channel blockers – Nifedipine, nitrendipine and verapamil.
• Nefedipine induces gingival enlargement in 20% of the cases.
Clinical features
• Begins as painless enlargement of one or two
interdental papillae.
• Increased stippling and a roughened or
pebbled surface with lobulations is presented.
• Dense, resilient and insensitive, no tendency to
bleed.
• No difficulties observed, although it is
aesthetically objectionable.
• Proliferation of fibrous connective tissue with
numerous fibroblasts.
• Cyclosporine induced enlargements are more
vascularized n have more amounts if plasma
cells and extracellular substance.
• Recurrence is common and regression is seen
if the drug is discontinued.
3. Enlargement associated with systemic factors
a) Conditioned Enlargement
• Caused by systemic condition of the patient, which exaggerates the usual gingival response
to dental plaque.
• They are of three types :
i. Hormonal
ii. Nutritional
iii. Allergic

i. Hormonal Enlargement
• May result from endocrine imbalance during the development of patient.
• Increased levels of oestrogen and progesterone in pregnancy cause change in vascular
permeability, leading to oedema an altered inflammatory response to dental plaque.
• Gingivitis in pregnancy is sometimes reffered as preganancy tumour.
• Microscopic features- increased vascularity, multiplication of fibroblasts, oedema and
infiltration of leukocutes.
ii. Nutirtional enlargement

Vitamin C deficiency
• Enlargement of gingiva – classic description of scurvy.
• Combined effect of vitamin c deficiency and
inflammation.
• Gingivae become tender, swollen and oedematous and
bleed on slightest provocation.
• Gingival sulci filled with partially clotted blood .
• Crests of interdental papillae are red or purple and
sometimes ulcerated and necrosed.
Treatment
• Improvement of oral hygiene and administration of
vitamin C.
Periodontitis
An inflammatory disease of the supporting tissues of the tooth caused by
specific microorganisms ,resulting in progressive destruction of the periodontal
ligament and alveolar bone with pocket formation ,recession ,or both.

Chronic periodontitis
{ periodontoclasia, pyorrhea, pyorrhea alveolaris, Schmutz pyorrhea }
• Most common form of periodontal disease and is associated with local
irritation.
• This begins as a marginal gingivitis, which usually progresses to chronic
periodontitis if untreated or improperly treated.
• Referred to as marginal periodontitis most common in adults.
Aetiology
• Local factors such as microbial plaque, calculus, food impaction and
irritating margins of fillings appears to be most important in the
development of this common form of periodontal disease.
• Predominantly associated with A. actinomycetemcomitans, Bacteriods
forsythus, Porphromonas gingivalis and Prevotella intermedia.
Clinical features
• Periodontitis usually begins as a simple marginal gingivitis, as a reaction to
plaque or calculus.
• It is a tiny ulceration of the crevicular epithelium.
• The gingiva becomes more inflamed and swollen.
• It proliferates as a result of the inflammation so that at this stage there is a
tendency for the epithelial attachment to extend or migrate apically on the
tooth. As it does so, it gets easily detached as its coronal potion.
• Through this process and because of the increased swelling of the marginal
gingiva, the gingival crevice gradually becomes deeper and is classified as
an early periodontal pocket.
• The presence of periodontal pockets measuring more than 3-4mm indicates
the destruction of periodontal ligament and alveolar bone resorption.
• Swelling and hyperemia of the gingivae there is also a tendency for them to
bleed readily.
• Halitosis is also present.
• As periodontitis becomes more severe, the teeth become mobile and give
off a rather dull sound and hurt when tapped with a metal instrument.
• Compressed air and instrument exploration will reveal that the tissue
detachment may be severe.
• The embrasures may be open because the interdental papillae are deficient.
• The normal festooning is not apparent , and the gingivae appear 'boggy'
because of hyperemia and edema; no stippling is detected and the gingival
tissues are smooth, shiny, and perhaps redder or bluer than normal .
• Gingival recession is a common phenomenon.
• Gingival recession often begins as a thin break in the free gingiva adjacent to
the center of a tooth, this is called a Stillman's cleft.
Histological features
• The enlarged free marginal gingiva is densely infiltrated with lymphocytes
and plasma cells.
• The crevicular epithelium shows various degrees of proliferation, and often,
tiny ulcerations.
• Early microscopic signs is the appearance of the osteoclasts on the surface
of the bony crest. they soon appear to lie in the little bays of bone
resorption known as HOWSHIP'S LACUNAE.
• More plaque is deposited in an apical direction on the tooth.
• More irritation of the free gingiva occurs.
• The epithelial attachment proliferates apically down on to the cementum of
the tooth and shows more ulceration.
• The alveolar crest of bone is resorbed further apically
• Principal periodontal ligament fibers become disorganized and detached
from the tooth.
• A periodontal pocket exists between the free gingiva and the tooth , to
depths from 2mm down , until finally the apex of the tooth is approached.
Radiographic Features
• The earliest change in the
periodontal bone is a blunting of
the alveolar crest due to the
beginning of bone resorption.
• There is a tendency for cupping
out of the interdental alveolar
bone.
• The periodontal ligament space
retains its usual thickness.
Treatment And Prognosis

• By careful complete periodontal treatment, the teeth involved by

periodontal disease can be saved if the bone loss has not been too
extreme, if irritants are removed by scaling and curettage and if pockets
are eliminated by surgical removed of the gingiva [gingivectomy], if
osseous deformities are eliminated and the tooth supporting tissues
are recontoured to a normal physiologic architecture, if occlusal forces
are balanced, and systemic factors are corrected .
Crevicular epithelium
• For reattachment to occur , this epithelium must be curetted away .
• since cementum can be deposited only by connective tissue, the presence
of epithelium interferes with the reattachment .
• The fresh bleeding connective tissue surface will form a blood clot in
contact with the root, which can organize and contribute to reattachment.
Mobility
• During the period of reorganization the tooth must be at least relatively
immobile, since motion tends to disturb the healing process and allow any
remaining crevicular epithelium to proliferate and reline the pathologic
pocket.
Inflammation
• Itself apparently interferes with reattachment , perhaps because
cementoblasts cannot develop in areas of inflammation.

Necrotic Cementum
• Is also a barrier to reattachment, since new cementum apparently will not
be deposited upon cementum that has been in contact with oral fluids
and suppuration for an appreciable time.
Aggressive Periodontitis
• Aggressive periodontitis is a destructive disease characterized by the
following:
• the involvement of multiple teeth with a distinctive pattern of periodontal
tissue loss;
• a high rate of disease progression;
• an early age of onset;
• and the absence of systemic diseases.
• This disease rather appears to be the result of a defect in immune
response rather than plaque and calculus deposition.
• Micro flora associated with this disease are
1. A. actinomycetmcomitans
2. P. gingivalis
Clinical features
Localized form:
• Occurs usually around puberty and has a strong familial tendency.
• It is localized to first molars and incisors.
• There is attachment loss in at least two permanent teeth, one of which is
the first molar.
• A striking feature to this disease is absence of clinical inflammation despite
the presence of a deep periodontal pocket.
Generalized form:
• This affects mostly in patients aged less than 30 years.
• Marked distinction between this and localized form is the presence of
large accumulation of plaque, calculus and gingival inflammation.
Radiographic features
• In localized form, vertical loss of alveolar bone is seen around the first
molar and incisor at around the age of puberty in otherwise healthy
patients.
• An arc shaped alveolar bone loss extends from the distal surface of the
second premolar to the mesial surface of second molar and there is a
widening of periodontal ligament space.
• In the generalized form, bone loss may range from the involvement of
one or two teeth to a maximum number of teeth.
Histological features
• These closely resemble the features of chronic periodontitis.

Treatment
• Antibiotics should be administered in combination with mechanical
removal of plaque and inflamed periodontal tissues.
• Periodontal surgery should be performed with prophylactic antibiotic
cover and postoperative usage of chlorhexidine mouth rinse.
• Periodic follow up is necessary, since there is possibility of reinfection.
Papillon-lefevre Syndrome
• It is an autosomal recessive disorder
characterized by cutaneous and oral
manifestations.
• Cutaneous- keratotic lesions of palmar
and plantar surfaces.
• Oral- aggressive periodontitis, leading
to severe destruction of alveolar bone
involving both deciduous and
permanent dentitions.
• Due to rapid bone loss, mobility and
pathological migration occurs.
Necrotizing Ulcerative Periodontitis
• Chronic periodontitis along necrotizing ulcerative gingivitis is grouped as
necrotizing periodontal diseases.
• It doesn’t always present with attachment loss
• This may show attachment, bone loss and may be associated with
immune response or malnutrition.
• This NUG maybe observed In HIV positive patients.
• In them, it causes ulceration and necrosis of gingiva with pain and
spontaneous bleeding, the exposed underlying bone then undergoes
rapid destruction.
Histological features
• Connective tissue – vascular engorgement, oedema and formation of
abscess cavity surrounded by a diffused collection of PMNLs.
• Epithelium – exhibits secondary changes in form of intra and
intercellular oedema, micro abscess formation and sometimes
ulceration.

Treatment
• Spontaneous rupture is common.
• The invading foreign material will be expelled along with pus.
Gingival abscess
• Gingival abscess is an acute, localized and painful lesion of sudden onset.
• Caused by sudden forceful penetration of any foreign object such as
bristle of tooth brush etc. deep into gingival tissue.

Clinical features
• Limited to marginal gingiva usually.
• Appears as reddish swelling with a
smooth and shiny surface.
• It becomes fluctuant and exhibits
pus discharges.
Histological features
• Connective tissue – vascular engorgement, oedema and formation of
abscess cavity surrounded by a diffused collection of PMNLs.
• Epithelium – exhibits secondary changes in form of intra and
intercellular oedema, micro abscess formation and sometimes
ulceration.

Treatment
• Spontaneous rupture is common.
• The invading foreign material will be expelled along with pus.
Lateral Periodontal Abscess
• This is directly related to a pre existing periodontal pocket.
• Bacteria multiply in the depth of the pocket and cause enough irritation
to form an acute abscess with exudation of pus.
• This may result in enough swelling to destroy the cortical plate of bone.
• If it still exists, it may lead abscess to balloon underlying tissues, forming
a ‘gum boil’ or parulis.

Clinical features
• It usually occurs in adults, rare in children.
• Most common cause is foreign bodies.
• Pain, foul taste, mobility of the involved tooth, tenderness over the
corresponding gingiva and lymphadenopathy are other symptoms.
• Clinical manifestation of abscess was the release of pus from the neck of
a loose deciduous tooth upon pressure.

Treatment
• Treatment of periodontal abscess is similar to that of an abscess
elsewhere.
• If the abscess doesn’t drain spontaneously through the gingival crevice
and is not treated, a fistula may develop to spontaneously release pus
onto the mucosal surface.
• Careful insertion of a dull probe into the pocket along the tooth will
usually induce drainage, and acute symptoms will subside.
• Extraction of tooth is advised after acute symptoms have subsided.