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ACUTE GINGIVAL INFECTIONS
CONTENTS
Introduction
Primary herpetic gingivostomatitis
Necrotizing ulcerative gingivitis (NUG)
Pericoronitis
Abscesses of periodontium
INTRODUCTION
An acute lesion is of sudden onset and short duration
and is painful.
They are manifested with severe pain along with
systemic manifestations
Thus these lesions must be treated at the earliest with a
proper treatment protocol.
Primary herpetic gingivostomatitis
HSV- type 1
Infants/ children younger than 6 yrs
Males=females
Primary infection asymptomatic
The virus ascends through the sensory or autonomic nerves and persists in the neuronal ganglia that innervate the site as a latent HSV
Sunlight, fever, trauma, stress , after oral surgical procedures
Secondary manifestations
Herpes labialis
Herpetic stomatitis
Herpes genitalis
Ocular herpes
Herpetic encephalitis
Early stage Late stage showing brownish crusted lesions
CLINICAL FEATURES
Intra-oral
Diffuse, erythematous, shiny involvement of the gingiva and adjacent oral mucosa
Varying degree of edema and gingival bleeding
Discrete spherical grey vesiclesPrimary herpetic gingivostomatitis
Rupture of vesicles and formation of ulcers after 24 hrs
Ulcers– small , painful, red, elevated, halo-like margin with depressed yellowish/greyish white central portion
Widely spread/clusters
7-10 days
No scarring
Soreness, difficulty in eating and drinking
Ruptured vesicles sensitive to touch, thermal changes, foods such as condiments and fruit juices
Infants show irritability and refusal to take food
Extra-oral
Cervical adenitis
Fever (101 ͦ -105 ͦ F)
Generalized malaise
HISTOPATHOLOGY
Virus targets epithelial cells
Ballooning degeneration (acantholysis, nuclear clearing, nuclear enlargement)
Tzanck cells
Fusing of infected cells
Formation of multinucleated cells and intercellular edema Formation of intraepithelial vesicles
Rupture
Secondary inflammatory response with fibropurulent exudate
Ulcers with central portion of acute inflammation and exudation surrounded by zone rich in engorged blood vessels
DIAGNOSIS Early diagnosis important (reducing symptoms and
recurrences)
History/clinical findings
Virus culture
Immunologic tests using monoclonal antibodies or DNA hybridization techniques
DIFFERENTIAL DIAGNOSIS
Erythema multiforme:
o More extensive vesicles with pseudomembrane formation on rupture
o Tongue more involved
o Skin lesions present
o Prolonged involvement may occur for weeks
Stevens-Johnson syndrome: rare form of EM characterized by hemorrhagic lesions in the oral cavity, hemorrhagic occular lesions and bullous skin lesions
Bullous lichen plannus:
Rare & painful condition
Large blisters on tongue & skin- rupture
undergo ulceration
Skin lesions + oral involvement
Prolonged indefinite course
Linear, grey, lacelike lesions of lichen
plannus inter-spread among bullous
eruptions
Desquamative gingivitis
Chronic condition
Diffuse involvement of gingiva
Varying degree of peeling of epithelium
Recurrent aphthous stomatitis
Small well defined round shallow
ulcers, yellowish grey central
areas & red halo
H/o previous mucosal ulcers is
dignostic, unknown etiology
No diffuse erythematous involvement of the gingiva, no acute toxic symptoms
COMMUNICABILITY
Contagious
Most adults develop immunity due to infection during
childhood – subclinical infection
Hence seen in infants & children
Recent studies have demonstrated HSV in periodontal
pockets (Slots J 2000)
TREATMENT
Consists of early diagnosis & immediate initiation of antiviral
therapy.
Antivirals :
o Acyclovir suspension 15mg/kg is given 5 times daily for 7
days (Amir et al,1997)
o It reduces days of fever, pain, lesion and virus shedding
o Acyclovir does not affect normal cells but inhibits DNA
replication in HSV infected cells
o Newer antivirals like Valacyclovir and Famicyclovir can
also be used
o <3 days– antiviral
o >3 days- (immunocompetent pt) limited value
Palliative measures:
o Removal of food debris, plaque and supra gingival
calculus
o NSAID (FEVER AND PAIN)
o Extensive periodontal therapy to be postponed
o Local /systemic antibiotics to prevent opportunistic
infection especially in immuno-compromised patients
o The patient must be informed that the disease is contagious,
thus precautions must be taken (vesicles –highest viral titer)
Supportive measures:
o Copious fluid intake
o Nutritional supplements
o Topical anesthetics while eating
Infection of fingers of health professional treating infected patients may occur and is known as Herpetic Whitlows
Necrotizing ulcerative gingivitis
Necrotizing Gingivitis, Necrotizing Periodontitis and
Necrotizing Stomatitis are the most severe inflammatory
disorders caused by plaque bacteria
They are rapidly destructive and debilitating
A distinction between these diseases has not always been
made in the literature
Microbial diseases affecting gingiva/ periodontium in the context of an impaired host response
Characterized by death and sloughing of tissues
HISTORY
Fourth century BC, Xenophon mentioned that Greek soldiers
were affected with “sore mouth” and foul-smelling breath
In 1778, John Hunter described the clinical findings and
differentiated ANUG from scurvy and chronic destructive
periodontal disease
ANUG occurred in epidemic form in the French army in the
19th century
In 1886, Hersch, a German pathologist, discussed some of
the features associated with the disease such as enlarged
lymph nodes, fever, malaise and increased salivation
In 1890s, Plaut and Vincent described the disease and
attributed its origin to fusiform bacilli and spirochetes
NOMENCLATURE
Ulceromembranous gingivitis
Acute necrotizing ulcerative gingivitis
Trench mouth
Vincent’s gingivostomatitis
Phagedenic gingivitis
Fusospirallary periodontitis
Plaut-Vincent stomatitis
CLINICAL FEATURES
Classification
Acute Subacute (Repeated remissions and exacerbations) Recurrent
Single tooth, group of teeth Entire mouth
NUP(long standing, severe immunosuppression)
NUS
Noma
ORAL SIGNS AND SYMPTOMS
Punched out, craterlike depressions at the crest of the interdental papilla
Can extend into the marginal gingiva, attached gingiva and oral mucosa
Grey pseudomembranous slough
Linear erythema
Removing slough exposes red, hemorrhagic, shiny surface which bleeds easily
Fetid odor
Metallic taste
Increased salivation/pasty saliva
Can be superimposed on chronic gingivitis/periodontitis
Recession rather than pocket formation
Constant radiating, gnawing pain that is intensified on eating spicy and hot foods and on chewing
Lesions extremely sensitive to touch
Low socioeconomic groups
Seasonal variations (Skach et al, 1970)
EXTRAORAL AND SYSTEMIC SIGNS AND SYMPTOMS Local lymphadenopathy
Fever
Increased pulse rate, leukocytosis, loss of apetite and general lassitude additionally seen in severe cases
Insomnia, constipation, GI disorders, headache and mental depression in children
OTHER SEVERE SEQUELAE
1) Fusospirochetal meningitis
2) Peritonitis
3) Pulmonary infection
4) Toxemia
5) Fatal brain abscess
6) Noma
CLINICAL COURSE
ACCORDING TO HORNING AND COHEN:
Stage 1 : Necrosis of tip of the interdental papilla (93%).
Stage 2 : Necrosis of entire papilla (19%)
Stage 3 : Necrosis extending to gingival margin (21%)
Stage 4 : Necrosis extending to attached gingiva (1%)
Stage 5 : Necrosis extending to buccal / labial mucosa (6%)
Stage 6 : Necrosis exposing alveolar bone (1%)
Stage 7 : Necrosis perforating skin and check (0%)
ACCORDING TO PINDBORG:
Stage 1: Erosion of only tip of interdental papilla
Stage 2: Lesion extending to marginal gingiva and causing
potentially a complete loss of papilla
Stage 3: Involving attached gingiva
Stage 4: Exposure of bone
HISTOPATHOLOGY
Microscopically the lesion is acute necrotizing inflammation of the gingiva, involving both the stratified squamous epithelium and the underlying connective tissue
Epithelium destroyed and replaced by meshwork of fibrin, necrotic epithelial cells and PMN’s and various types of microorganisms (surface pseudomembrane)
Border: Epithelium edematous and individual cells exhibit varying degree of hydropic degeneration along with infilteration of PMN’s in the intercellular spaces
Underlying connective tissue: hyperemic with numerous engorged capillaries and dense infiltration by PMN’s (linear erythema)
Plasma cells at the periphery(underlying chronic condition)
Epithelium and CT alterations decrease with increase in distance from the necrotic area and gradually blends with the uninvolved area
Listgarten – described four zones that blend with each other
ZONE I - BACTERIAL ZONE- The Most superficial zone
Consists of varied bacteria, including a few spirochetes of
small, medium and large type.
ZONE II – NEUTROPHIL RICH ZONE - Contains
numerous leukocytes, predominantly neutrophils, with
bacteria, including many spirochetes of various types,
between the leukocytes
ZONE III – NECROTIC ZONE- Consists of disintegrated
tissue cells, fibrillar material, remnants of collagen fibers and
numerous spirochetes of the medium and large types, with
few other organisms
ZONE IV – SPIROCHETAL INFILTRATION ZONE-
Consists of well preserved tissue infiltrated with medium and
large spirochetes without other organisms.
Spirochetes have been found as deep as 300 microns from the
surface
ETIOLOGY
Role of bacteria
o Plaut and Vincent in 1894 and 1896, respectively
introduced the concept NUG is caused by specific
bacteria – namely a fusiform bacillus and a spirochetal
organism.
o Fusiform bacilli and a spirochetal organism are always
found in the disease.
Rosebury and coworkers described a fusospirochetal complex consisting of T. marcodentium, intermediate spirochetes, vibrios, fusiform bacilli and filamentous organisms in addition to several Borrelia species
More recently Loesche and colleagues described a constant
flora and a variable flora
Constant flora :- Fusospirochetal organisms, P.
intermedia, A. odontolyticus and
various spirilla like Selenomonas
species.
Variable flora :- Heterogenous array of bacterial
types
Bacteriologic findings have been supported by immunological data presented by Chung et al who reported increased IgG and IgM antibodies to intermediate spirochetes, P. intermedia in NUG patients as compared to those with chronic gingivitis and healthy controls
Metronidazole effective
Role of host response
Presence of organisms insufficient to cause disease
NUG is not produced experimentally in humans and animals by inoculation of bacterial exudates from the lesion
Characteristic lesions occurs in animals when they are under immunosupression
Not found in well nourished individuals with fully functional immune system
Immunosupression essential- NUG patients displayed depression in leukocyte chemotaxis and phagocytosis (Cogen et al, 1983)
Nutritional deficiency, fatigue caused by chronic sleep
deprivation, alcohol/drug abuse, psychological factors, systemic disease
It is hence concluded that -
The specific cause of NUG has not been established & it is
produced by a complex of bacterial organisms but requires
underlying tissue changes to facilitate the pathogenic
activity of the bacteria. HIV
LOCAL PREDISPOSING FACTORS
Pre-existing gingivitis
Injury to the gingiva (eg: malocclusion)
Smoking
98% pts with NUG were smokers & frequency of the disease increases with increasing exposure to tobacco smoke (Pindborg et al, 1951)
Preexisting chronic periodontitis, pericoronal flaps (favourable environment for anaerobic fusiform bacilli and spirochetes)
SYSTEMIC PREDISPOSING FACTORS
Nutritional deficiency
Produced in animals by giving them nutritionally deficient diet
Nutritional deficiencies diminishes immune responses and alteres the periodontal structures, making them more susceptible
Debilitating disease
Chronic diseases( syphilis, cancer)
Severe gastrointestinal disorders (ulcerative colitis)
Blood dyscrasias( anemia, leukemia)
AIDS
Psychosomatic factors
Disease often occurs in association with stressful situations (induction into the armed forces, school examinations)
Hypothalamic-pituitary-adrenal axis activation resulting in cortisol secretion and decrease in immune response
Increase in the levels of cortisol and catecholamines
leads to reduced gingival microcirculation and salivary
flow which enhances nutrition to P.intermedia
Depression in neutrophil and lymphocyte function leads
to bacterial invasion and tissue damage.
(Johnson and Engel 1986)
DIAGNOSIS
Clinical findings (gingival pain,ulceration and bleeding)
Bacterial smear not definitive
Microscopic examination of biopsy specimen (TB, neoplastic disease)
DIAGNOSTIC CRITERIA
By Genco, Goldman and Cohen:
Interproximal necrosis and ulceration (punched-out papillae)
Painful gingiva
Bleeding (spontaneous or on slight provocation)
Pseudomembrane (fibrin, debris)
Fever, malaise, lymphadenopathy
“Fetor Oris”
Herpetic Gingivostomatitis
Chronic Periodontitis
Desquamative Gingivitis
Streptococcal Gingivostomatitis
Apthous Stomatitis
Diptheric And Syphilitic Lesions
Tuberculous Gingival Lesion
Candidiasis
Agranulocytosis
Dermatoses (Pemphigus, Erythema Multiforme ,Lichen
Planus)
Treatment differs Herpes/NUG
STREPTOCOCCAL GINGIVOSTOMATITIS
Characterized by diffuse erythema of the gingiva and other
areas of the oral mucosa
Necrosis of the gingival margin – not a feature of this
disease.
No fetid odor
Bacterial smears– streptococcal forms
Streptococcus viridans , groupA ß-hemolytic streptococcus
GONOCOCCAL STOMATITIS
Caused by Neisseria gonorrhoeae
Mucosa is covered with a grayish membrane that sloughs
off in areas to expose an underlying raw bleeding surface
Most common in new born due to transmission through
maternal passages
AGRANULOCYTOSIS
Characterized by marked decrease in number of circulating
PMN’s
Lesions similar to NUG
No marked inflammation due to diminished defense mechanism
Blood studies can be used to differentiate between NUG and
agranulocytosis
VINCENT’S ANGINA
Fusospirochetal infection of oropharynx and throat,
distinguished from NUG, which affects marginal gingiva.
May extend to the larynx and the middle ear
NUG in Leukemia
Not produced by leukemia per se , but due to reduced
host defense mechanism
NUG may superimpose on gingival tissue alteration
caused by leukemia
NUG IN HIV PATIENTS
Same clinical features
Extremely destructive course leading to NUP
Presenting symptom for HIV
COMMUNICABILITY
Not contageous
Study by King
Kitchen facilities (controlled conditions, anaerobic environment, do not survive on utensils)
Occurrence in epidemic like outbreaks– due to common predisposing factors
Immunosupression+bacteria
NUP Extension of NUG or different disease entity
No evidence
Clinical similarities
Until distinction can be proved/disproved, classified together
Classification first adopted in world workshop in clinical periodontics in 1989
Deep interdental osseous craters
Recession
HIV positive patients
Strongly associated
Marker of immune supression and diagnosis of AIDS
HIV-P
Aggressive form of chronic periodontitis
TREATMENT
Alleviation of the acute symptoms by reducing microbial load
and removal of necrotic tissue
Treatment of chronic disease either underlying the acute
involvement or elsewhere in the oral cavity
Alleviation of the generalized symptoms such as fever
and malaise
Correction of the systemic conditions that contribute to
the initiation or progression of gingival changes.
SEQUENCE OF TREATMENT FIRST VISIT
Complete evaluation
Comprehensive medical history with special attention to recent illness, living conditions, dietary backgrounds, type of employment, hours of rest, cigarette smoking, stress levels, HIV
Examination should include general appearance, presence of halitosis, skin lesions, vital signs, lymph nodes
o Characteristic lesions
o Oral hygiene (Pericoronal flap Pockets Local irritants)
o Only acutely involved areas
o Isolated with cotton rolls and dried
o Topical anesthetic
Area swabbed to remove pseudo membrane with moistened
cotton pellet after 2-3 min
Cleanse area with warm water
Superficial calculus removed (ultrasonic scalers)
Subgingival scaling and curettage – contraindicated
(bacteremia, extend infection to deeper tissues)
Surgical procedures other than emergencies postponed until pt is symptom free for 4 weeks
Antibiotic regimen (amoxicillin 500 mg orally every 6 hrs for 10 days) in moderate to severe cases
Metronidazole (500mg BID 7 days)
Emergency procedures along with systemic antibiotics
PATIENT INSTRUCTIONS
Patient told to rinse every two hours – glass full of equal mixture of warm water and 3 % Hydrogen peroxide and / or twice daily with 0.12%chlorhexidine
Adequate rest
Confine toothbrushing to removal of surface debris, ultrasoft brush, bland dentrifice
Analgesics
Avoid tobacco, alcohol, condiments
Report back in 1-2 days
Motivation
SECOND VISIT Patient condition – usually improved. Pain is diminished
or no longer present.
Areas still erythematous but without pseudomembrane
Shrinkage of gingiva – expose calculus which is then
gently removed.
Instruction same as previous visit
THIRD VISIT
5 days after 2nd visit
Patient should be symptom free
Repeat scaling and root planing
Discontinue hydrogen peroxide mouthwash but continue CHX
mouthwash
Patient instructed in plaque control procedures
Councelling on nutrition, habits
SUBSEQUENT VISITS Tooth surfaces in the involved areas are scaled.
Plaque control is checked and corrected if required.
Patient should now be scheduled for treatment of chronic
disease.
GINGIVAL CHANGES WITH HEALING
Removal of pseudo membrane – exposes red crater like
hemorrhagic depression.(loss of normal barrier function
of epithelium)
Next day: Bulk and redness of crater margins reduced –
but surface shiny.(reduction in inflammation and
reepithelization)
Early signs of restoration of normal gingival contour and
color. (further reduction in inflammation, reestablishment of
normal barrier function including keratinization)
Final stage- Normal gingival contour, colour, consistency are
restored. Portions of roots exposed are covered by healthy
gingiva
ADDITIONAL TREATMENT CONSIDERATIONS
Countouring of gingiva as adjunctive procedure Shelf like margin Unesthetic, favours plaque retention
Systemic antibiotics/topical antimicrobials Only in pts with systemic complications and local adenopathy Drug therapy—adjunctive to local debridement
Supportive systemic treatment
Copious fluid consumption
Administration of analgesics
Bed rest
Nutritional supplements
RATIONALE
Lesions similar to NUG have been produced in animals –
with certain nutritional deficiencies
Difficulty in chewing raw fruits and vegetables may lead
to selection of diet deficient in Vit B and C.
Fewer recurrences – local treatment of NUG is
supplemented by Vit B or C.
Supplements may be discontinued after two months
PERSISTANT OR RECURRENT CASES
Reassessment of differential diagnosis to rule out diseases that resemble NUG
Underlying systemic disease causing immunosupression (HIV)
Inadequate local therapy (mandibular anterior area due to pericoronal infection)
Inadequate compliance
Pericoronitis
Abscesses of the periodontium
ACUTE GINGIVAL INFECTIONS-ӀӀ
CONTENTS
Introduction
Primary herpetic gingivostomatitis
Necrotizing ulcerative gingivitis/ periodontitis (NUG)
Pericoronitis
Abscesses of periodontium
Conclusion
References
Pericoronitis
Inflammation of the gingiva in relation to the crown of an incompletely erupted tooth
Mandibular third molar area
Acute
Subacute
Chronic
PATHOGENESIS Space- ideal area for
accumulation of food debris and bacterial growth
Inflammatory fluid and cellular exudate
Increase in bulk of the
flap
Interferes with complete closure of
jaws or can be traumatized by
contact with opposing jaw
Aggrevation of the
inflammatory involvement
CLINICAL FEATURES
Chronic – no clinical signs or symptoms (chronic inflammation and ulceration on inner surface)
Acute (trauma, occlusion, foreign body impaction)
Inflammatory involvement +systemic complications
Red swollen suppurating lesion
Tender
Radiating pain to ear, throat, floor of mouth
Foul taste
Inability to close jaws
Swelling of cheek, lymphadenitis, trismus
Fever, leukocytosis, malaise
COMPLICATIONS Localized- pericoronal abscess
Spread- submaxillary, posterior cervical, deep cervical and retropharyngeal lymph nodes
Peritonsillar abscess, cellulitis, Ludwig’s angina
Pericoronal abscess Peri-tonsillar abscess Ludwig’s angina
TREATMENT
Severity of inflammation
Systemic complications
Retaining/extracting involved tooth
Chronic pericoronitis Removal as a preventive measure
Acute pericoronitis Flushing area with warm water to remove debris and
exudate
Swabbing with antiseptic after elevating the flap gently
Occlusal adjustment
Abscess drainage
Antibiotics
Decision to retain or extract the tooth after acute symptoms subside
Decision governed by likelihood of further eruption into good functional position, bone loss distal to second molars
Extraction- Early extraction before root formation is completed
Retaining tooth- removal of pericoronal flap using periodontal knives or electrosurgery
incorrect
correct
healed site
Surgical procedure to remove operculum
Abscesses of the periodontium
DEFINITION
Periodontal abscess is defined as a lesion with expressed periodontal breakdown occuring during a limited period of time and with easily detectable clinical symptoms, and localized accumulation of pus within the gingival wall of the periodontal pocket (Hafstrom et al, 1994)
Independent disease entity (AAP world workshop, 1999)
Represents period of active tissue breakdown due to extension of infection into intact periodontal tissues
CLASSIFICATION
According to location (Meng et al, 1999) Gingival abscess Periodontal abscess Pericoronal abscess
According to clinical signs and symptoms Acute abscess Chronic abscess
According to number Single Multiple (diabetes, immunosupression)
Localized periodontal abscess in pt with poorly controlled type 2 diabetes mellitus
According to aetiologyA) Periodontitis related abscess
1) Exacerbation of chronic lesion
2) Post therapy periodontal abscess
a) Post scaling periodontal abscess (Dello Russo, 1985)—calculus impaction or obstruction
b) Post surgery periodontal abscess (Garrett et al, 1997)– foreign body reaction, incomplete removal of calculus
c) Post antibiotic periodontal abscess (no mechanical therapy, superinfection)
Post scaling abscess
B) Non periodontitis related abscess
1) Impaction of foreign body in gingival sulcus
2) Root morphology alterations– invaginated root, fissured root, external root resorption, root tears, iatrogenic endodontic perforations
GINGIVAL ABSCESS
Localized acute inflammatory lesion that may arise from a variety of sources such as microbial plaque infection, trauma and foreign body impaction
Red, smooth, fluctuant, painful
Marginal gingiva/interdental papilla
PERICORONAL ABSCESS
o Associated with operculum of partially erupted tooth
o Mandibular 3rd molars most frequently affected
PERIODONTAL ABSCESS
A localized purulent infection within the tissues adjacent to the periodontal pocket that may lead to the destruction of periodontal ligament and alveolar bone
In patients with untreated periodontitis
Moderate to deep pockets
Acute exacerbation of chronic condition
Incomplete calculus removal, antibiotic therapy, periodontal surgery
Occlusion due to deep tortuous pocket, tooth morphology, debris, closely adapted pocket epithelium
ACUTE ABSCESS Exacerbation of chronic condition due to increase in number or
virulence of bacteria combined with lowered tissue resistance and lack of spontaneous drainage
Exudation
Sensitivity to percussion
Pain, Mobility
Tooth elevation in socket
Systemic involvement
CHRONIC ABSCESS Forms when spreading infection has been controlled by
spontaneous drainage, host response or therapy
No/dull pain
Fewer/no symptoms
Fistulous tract
No systemic involvement
Periodontal Vs. Periapical Abscess
Periapical Abscess
•Non-vital tooth
• Caries, restoration
• No pocket
• Apical radiolucency
• No or minimal mobility
• Percussion sensitivity
• Sinus tract opens via
alveolar mucosa
•Severe, diffuse pain
Periodontal Abscess
•Vital tooth
• No caries
• Pocket, bone loss
• Lateral radiolucency
• Mobility
• Percussion sensitivity variable
• Sinus tract opens via
keratinized gingiva
•Dull localized pain
PREVALENCE 8-14% among all dental conditions
needing emergency treatment (Ahl et al, 1986)
Positively correlated with pocket depth
High prevalence in molars- 50% (Smith and Davies, 1986)
3rd most frequent dental emergency
PATHOGENESIS AND HISTOPATHOLOGY
Contains bacteria, bacterial products, inflammatory cells, tissue breakdown products and serum
Occlusion of pocket lumen, extension of infection into soft tissues
Entry of bacteria into soft tissue pocket wall
Accumulation of leukocytes, connective tissue destruction, bacterial encapsulation, formation of pus
Central area
Rate of tissue destruction depends on– growth and virulence of bacteria, Ph
MICROBIOLOGY
Polymicrobial, mainly caused by endogenous bacteria (Tabaqhali, 1988)
Similar to flora of chronic periodontitis
Domination by gram negative, non-motile, strict anaerobic, rod-shaped species
Pg
Pi, Tf, Fn, spirochetes (anaerobic species)
Bifidobacterium spp, Actinomyces spp (gram positive, strict anaerobic)
Aa, Capnocytophaga spp, Campylobacter spp (gram negative, facultative anaerobic)
DIAGNOSIS
Clinical signs and radiological signs
Ovoid elevation on lateral side of root
Fistula, suppuration
Pain, tenderness, swelling
Sensitivitry to percussion
Mobility, tooth elevation, pocket
Bone loss
Systemic effects
Use of dark field microscopy ( Trope et al, 1988)
PET (Liu, 1996)
DIFFERENTIAL DIAGNOSIS Periapical abscess
Lateral periapical cyst
Vertical root fractures
Endo-perio abscesses
Parrish et al (1989)- 3 cases of osteomyelitis
TREATMENT1) Resolving acute lesion
2) Management of the resulting chronic condition
ACUTE ABSCESS Drainage through pocket retraction or incision
Scaling/ root planing
Periodontal surgery
Short term high dose adjunctive systemic antibiotics
Tooth removal
Avoid aggressive mechanical instrumentation in initial stage
Reduce exertion
Fluid intake
Chlorhexidine mouthwash
Warm saline gargles
Analgesics/antibiotics
Chronic abscess SPT, surgery/ antibiotics
Gingival abscess Scaling/ root planing Drainage Removal of cause Warm saline gargles
Pericoronal abscess
Drainage
Irrigation to remove debris
Warm saline gargles, antibiotics
Analgesics
Operculectomy/ extraction
COMPLICATIONSA) Tooth loss
B) Dissemination of infection1) Dissemination of bacteria inside the tissues during
therapy
2) Bacterial dissemination through blood stream due to bacteriema from an untreated abscess
Pulmonary actinomycosis
Brain abscess
Cellulitis
Cervical necrotizing fasciitis
Necrotizing cavernositis
CONCLUSION
Acute gingival infections lead to severe discomfort and may lead to life-threatening complications, and therefore they need to be treated promptly
Adequate patient education and motivation is necessary as patients do not complete the treatment once the acute phase has subsided
REFERENCESo Newman, Takei, Klokkevold, Carranza: Carrazanza’s Clinical
Periodontology, Saunders, 10th edition.
o Acute necrotizing ulcerative gingivitis: risk factors involving host defense mechanisms.-- Yoji, Hidemi, Atsushi: Periodontology 2000, Vol. 6, 1994, 116-124.
o Burkitt – Textbook of oral medicine
o Shafer –Textbook of oral pathology
o Lindhe, Lang, Karring: Clinical Periodontology and Implant Dentistry. Blackwell Munksgaard, 5th edition.
o The Periodontal abscess– A Review: Herrera et al, JCP 2000; 27: 377-386