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Good morning…….
ACUTE GINGIVAL INFECTION
Sudden onset of a conditionAcute
Gingival Relating to the gums
Infection Pathological state resulting from the invasion of the body by pathogenic microorganisms
Sudden onsetLimited durationWell defined clinical features
Infection or lesion
Affect gingiva
ACUTE GINGIVAL INFECTION
1) Traumatic lesions-physical and chemical2) Viral infections
• Acute herpetic gingivostomatitis• Herpangina• Hand, foot and mouth disease• Measles• Herpes varicella/zoster virus infections• Glandular fever• HIV infection
3) Bacterial infections• Acute necrotizing ulcerative
gingivitis• Tuberculosis• Syphilis
4) Fungal infections• Candidiasis
5) Gingival abscess6) Aphthous ulceration7) Pericoronitits8) Erythema multiforme9) Drug allergy and contact
hypersensitivity
ACUTE ACUTE HERPETIC HERPETIC
GINGIVOSTOMATITIS GINGIVOSTOMATITIS
• Caused by herpes simplex virus type 1 (HSV-
1).
• Ectodermal structures- Affected.
• Age-below 6 years.
• No sex predilection.
• Contagious.
Latency of herpes simplex virus
Oral signs
• Diffuse, erythematous, shiny involvement of gingiva and adjacent oral mucosa.
• Edema and gingival bleeding.
• Gray fluid filled vesicles: Rupture after 24 hrs & form ragged painful ulcers covered by yellowish or gray membrane and surrounded by an erythematous halo.
• Ulcers heal in 7-10 days without scarring.
Oral symptoms
• Soreness.
• Ruptured vesicles : Painful and sensitive to touch, thermal changes, fruit juices and coarse food.
• Infants: Irritability and refusal to take food.
Extra oral signs and symptoms
• Cervical adenitis
• Fever (101º F- 105º F)
• Malaise
• Headache
Histopathology
• Intraepithelial blister.• Ballooning degeneration of cells.• Lipschütz bodies.• Tzanck cells.• Connective tissue : Inflammatory cells.• When vesicles rupture - Surface is covered by
exudateFibrin, PMN and degenerated cells
Diagnosis
• Patient history and clinical findings.
• Direct smear finding
• Viral isolation and identification.
• DNA hybridization.
• Immunofluorescent staining of smears.
Differential diagnosis
• Necrotizing Ulcerative Gingivitis
• Erythema multiforme
• Stevens-Johnson syndrome
• Bullous lichen planus
• Desquamative gingivitis
• Recurrent apthous stomatitis.
Complications of HSV infections
• Herpetic whitlow
• Herpetic eczema
• Herpetic keratoconjunctivitis
• Act as a causative agent for erythema multiforme.
• Fatal encephalitis.
Treatment
• Early diagnosis and immediate initiation of antiviral therapy.
• Symptomatic and supportive
• Severe cases-Acyclovir therapy
: 200 mg 5X a day for 5 days
: 5 ml suspension 5Xa day for 5 days
: Acyclovir cream (apply 5X a day)
Palliative care
• Removal of plaque and food debris.
• NSAID (Fever and pain).
• Nutritional supplements.
• Topical anesthetics before eating.
• Local or systemic antibiotics to prevent secondary infection.
HERPANGINA
•Coxsackie A(1-6,8,10,16,22)
•Rarely affects gingiva
(causes ulceration & sore
throat)
•Heals in 7-10 daysHAND, FOOT AND MOUTH DISEASE
•Coxsacke A (16 , 5 or 6)
•Oral vesicles > small ulcers
•Heals in 10-14 days
Anterior faucial walls
HERPES ZOSTER VIRUS INFECTIONS
• Small vesicles seen on gingiva and tongue
• Recovery in 2-3 weeks
• Caused by reactivation of latent virus or reinfection
• Affect sensory nerve neuralgia
GLANDULAR FEVER
• Epstein Barr virus infection
• Acute gingivitis and stomatitis
• Widespread lymphadenopathy
• Can progress to ANUG
• Good oral hygiene and professional cleaning important
HIV INFECTION
Caused by HIV or Human Immunodeficiency
virus
HIV 1
Most common, seen
through out the world
• Both direct and indirect effects on oral mucosal immunity
• Affect both cellular and humoral immunity & both specific and innate immunity.
S.J.Challacombe, J.R.Naglik (2006)
HIV 2
West Africa +
Western &
Southern India
CD4 count (/c mm)
Asymptomatic
Symptomatic
AIDS indicator condition
>500 A1 B1 C1
200-499 A2 B3 C2
<200 A3 B3 C3
1993 CDC CLASSIFICATION
A3, B3, C3, C1, C2 are AIDS
GINGIVAL LESIONS
• Rare , multifocal , vascular neoplasm
• Malignant tumor ( localized & slowly growing lesion )
• Etiology: Activation of the latent HHV-8
• In HIV + ve : converts the diagnosis into AIDS.
KAPOSI’S SARCOMA
CANDIDIASIS
• Caused by Candida Albicans: Oppurtunistic infection
1)Acute Pseudomembranous
candidiasis( Thrush):
• Creamy white elevated patches, can be wiped away leaving a raw red base
• Painless or slightly sensitive
• Sore dry mouth or throat
2)Erythematous candidiasis
3) Angular Chelitis:
4) Hyperplastic candidiasis:
Doesn’t effect
LINEAR GINGIVAL ERYTHEMA :
• Erythematous gingival band, dark or fiery red in color, that often extends into attached gingiva. Plaque is minimal
• Does not respond to treatment
• Localized or generalized
• Can serve as a precursor for NUP
NECROTIZING ULCERATIVE GINGIVITIS
•Extremely destructive course leading to NUP
•CD4+ cell counts < 100 cell per mm3.
Bacterial infections
• Acute necrotizing ulcerative gingivitis
• Tuberculosis
• Syphilis
NECROTIZING ULCERATIVE NECROTIZING ULCERATIVE GINGIVITISGINGIVITIS
A rapidly destructive, noncommunicable, gingival infection of complex etiology
400 B.C. Historical war of Xenophon’s troop
Soldiers of the Greek armyRoman Army: 1st Century A.D
HISTORY
SYNONYMS
• Acute ulceromembraneous gingivitis
• Trench mouth
• Cheilokake
• Phagedenic gingivitis
• Ulcerative gingivitis
• Vincent’s stomatitis
• Plant-Vincent’s stomatitis
•Stomatitis ulcerosa
•Fusospirillary gingivitis
•Fetid stomatitis
•Putrid stomatitis
•Acute septic gingivitis
•Pseudomembranous
angina
•Spirochetal stomatitis
SYNONYMS
CLASSIFICATION
• Acute disease
• Subacute disease
• Recurrent disease
• Chronic disease
PATIENT HISTORY
• Sudden in onset
• Following debilitating disease or acute respiratory tract infection.
• Change in living habits
• Inadequate rest, stress, poor nutrition, tobacco use.
ORAL SIGN
• Punched out craters
- Crest of interdental papilla
- Covered by gray pseudomembrane.
• Linear erythema.
• Gingival hemorrhage
- Spontaneous or slight provocation.
•Fetid odor.
•Increased salivation.
•Can occur in disease free mouth or superimposed on chronic gingivitis.
•No pocket
ORAL SYMPTOMS
• Lesions are sensitive to touch
• Constant radiating, gnawing pain
• Metallic foul taste in the mouth
• Pasty saliva
EXTRA ORAL SIGNS AND SYMPTOMS
• Local lymphadenopathy.
• Elevated temperature.
• Increased pulse rate.
• Leukocytosis.
• Loss of appetite.
EXTRA ORAL SIGNS AND SYMPTOMS
•GeneraL lassitude.
•Insomnia, headache, mental depression.
•GIT disorder, constipation.
•Head ache & mental depression
CLINICAL COURSE
NECROTIZING ULCERATIVE GINGIVITIS
NECROTIZING ULCERATIVE PERIODONTITIS
SYSTEMIC COM PLICATION
STAGING OF ANUG
Pindborg et al 1966
1.Erosion at tip of the interdental papilla.
2. Marginal gingiva involved (punched out papilla).
3. Attached gingiva affected.
4. Bone is exposed.
Staging of oral necrotizing diseases
Horning and Cohen 1995
Stage 1: necrosis of the tip of interdental papilla (93%) -NUG
Stage 2: necrosis of the entire papilla (19%)-NUG/NUP
Stage 3: necrosis extending to the gingival margin (21%)-NUP
Stage 4: necrosis extending to the attached gingiva (1%)- NUP
Stage 5: necrosis extending into buccal or labial mucosa (6%)- Necrotizing stomatitis
Stage 6: necrosis exposing alveolar bone (1%)- Necrotizing stomatitis
Stage 7: necrosis perforating skin of cheek (0%) - NOMA
STAGING OF ANUG
HISTOPATHOLOGY
• Epithelium : :Destroyed
: Replaced by meshwork of fibrin, necrotic epithelial cells, PMNs and microorganisms.
• Cells : Hydropic degeneration
•Connective tissue :: Hyperemic
: Engorged blood vessels : Dense infiltration of PMNs : Numerous plasma cells at the periphery.
ETIOLOGY
• Plaut 1894 and Vincent 1896- fusiform bacillus and spirochetes.
Fusiform bacillus:
• Gm +ve anaerobe rod • 5- 14 µm in length• 0.5 -1.0 µm in diameter• Non motile
Borrelia vincentii:
•Gm -ve spirochete•3–6 long loose spirals•10-15 µm in length•Motile organism
•Loesche et al 1982:
Constant flora : P. intermedia, Fusobacterium, Treponema & Selenomonas Variable flora : Heterogeneous bacteria.
•Chung et al 1983 :
Higher IgG and IgM levels to intermediate sized spirochetes and P.intermedia
Relation of bacteria to the characteristic lesion
Listgarten 1965
• Zone 1:• Zone 2: • Zone 3: • Zone 4:
Cocci and rods in addition to the spirochetes within the adjacent non-necrotic connective tissue region was found. (Courtois 1983)
Spirochetal infiltration
Necrotic zoneNeutrophil rich zone
Bacterial zone
ROLE OF HOST RESPONSE
• Depression in PMN chemotaxis and phagocytosis. (Cogen et al 1983)
• CD4:CD8 ratio is inversed. (Enwonwu 1994)
• Dysregulated cytokine production (Enwonwu et al 2005)
Predisposing factors1. Local factors Preexisting gingivitisInjury to gingivaSmoking
2. Systemic factorsNutritional deficienciesDebilitating disease
3. Psychosomatic factors
Predisposing factors
References
Pathogenesis
Emotional stress
Cohen-Cole et alSchoor & HavrillaJohnson & EngelMelnick et al.
Increased steroid levels depress immune defense systems.
Smoking Cohen-Cole et alKowolik & NesbetClarke et alJohnson & EngelMelnick et al.
Nicotine exposure initiates vasoconstriction resulting in relative ischemia contribute to tissue destruction.
Systemic diseases
Ryan et alDeasy et alJaworsky et al.
Cancer (immunosuppression)Von Willebrands disease (coagulation disorder; SLE, HIV infection
Altered immune systems
Chung et alCogen et alClaffey et alCogen et al.
Humoral antibody: high serum IgG or IgM levels to spirochetes and P.intermedia; Cell mediated immnity:Depressed Neutrophil & Lymphocyte activitylow CD4+/CD8+ ratio due to high CD8+ level.
Prevalence • Occurs at all age with highest incidence b/w
20-30 yrs (Dean 1945).
• Common in children from low SES in underdeveloped countries.
• In India, Pindborg JJ, Bhat M, Devnath KR in 1966 concluded that 58% of the patients were younger than 10 yrs.
• Common in children with Down syndrome than in other mentally retarded children.
Communicability
• Disease associated with the fusospirochetal bacterial complex is transmissible but has not been shown to be communicable or contagious.King 1943
Diagnosis
• Gingival pain• Ulceration• Bleeding
• Important to identify the underlying predisposing factors.
DIFFERENTIAL DIAGNOSIS
Streptococcal gingivostomatitis• Diffuse erythema. • No necrosis.• No fetid odor.
Agranulocytosis
• No inflammation. • Blood investigation can differentiate from NUG.
Vincent’s angina • Fuso-spirochetal infection of oropharynx and
throat.
TREATMENT
First visit
History
Examination-
• Intra-oral• Extra-oral• General
Start treatment
Treatment
• Reduction of microbial load :
Removal of pseudomembrane & nonattached
surface debris and superficial calculus.
• Avoid extraction or surgery until 4 weeks after acute
symptoms subsides.
• Antimicrobial therapy (systemic symptoms)
Instructions to the patient • Avoid-
• Mouth rinse:: 1:1 3% H2O2 and warm water 2 hourly or
0.12% CHX mouthwash.
3%Hydrogen peroxide
( 50 % dilution in warm non irritating solution)
1. Effervescence action:: Mechanical cleansing (Nascent oxygen bubbles going
away) : Highly significant
Mechanism of action:
2. Oxidative prperty:
H2O2
H2O+0 [Nascent oxygen]
Other reactive oxygen species produced:superoxide and hydroxyl radical
(More powerful)
(Davidson and Branen, 1993)
Catalase & Peroxidase
BactericidalAnaerobic bacteria
Second visit (1 to 2 days later)
• Evaluate patient for signs and symptoms.
• Gingival margins : Erythematous but without superficial pseudomembrane.
• If sensitivity permits- Scaling is done
• Shrinkage of gingiva- May expose previously covered calculus – Remove gently.
Third visit (5 days later)
• Patient should be symptom free.
• Scaling and root planing are repeated.
• OHI reinforced.
• Patient counseling.
• H2O2 mouthwash is discontinued, but CHX rinses can be maintained for 2-3 weeks.
Subsequent visits
•Tooth surfaces in the involved areas are scaled and smoothened.
•Further periodontal therapy if required
•Patient should be reevaluated at 1 month
Additional treatment considerations
• Gingival contouring
• Antimicrobials therapy
• Supportive systemic treatment
• Nutritional supplements- vit C, A and B complex.
Persistent or recurrent cases
• Reassessment of differential diagnosis
• Underlying systemic disease causing immunosuppression
• Inadequate local therapy
• Inadequate compliance
SEQUELAE OF INADEQUATE TREATMENT
•NOMA (Cancrum Oris, gangrenous stomatitis, running horse gangrene)•Fusospirochetal meningigits•Peritonitis•Pulmonary infections•Toxemia•Brain abscess •Necrotizing stomatitis•Recurrent infection
TUBERCULOSIS:
•specific granulomatous infectious disease
•extremely rare and forgotten entity
•Gingival lesion: Secondary to primary tuberculosis
•Lesion: Nodules, Deep ulcers, or Elevated fissures
SYPHILIS
•Primary: Ulcer
•Secondary (More common)
: Mucous patches, Snail track
ulcers
: Vesiculobulous lesions
•Tertiary: Gumma (rarely)
FUNGAL INFECTION
1.Acute pseudomembranous candidiasis
2.Acute atrophic candidiasis
3.Chronic atrophic candidiasis
4.Oro-pharyngeal candidiasis
ACUTE ACUTE GINGIVAL ABSCESSGINGIVAL ABSCESS
Abscess confined to the gingiva
May discharge spontaneously
Spread into underlying tissue
Periodontal abscess
Clinical features• Localized, painful, rapidly expanding lesion
with sudden onset.
• Limited to marginal and interdental papilla.
• Initially- red swelling with shiny surface.
• Fluctuant and pointed with a surface orifice (24-48 hrs)
• Adjacent teeth sensitive to percussion.
• Ruptures spontaneously.
Etiology
• Forceful impaction of foreign substance into gingiva.
• Trauma.
• Bacteria carried deep into tissues.
Epithelium : Intra and extracellular edema, leukocytes invasion and ulceration.
Edematous tissue with vascular engorgement
PMNs
Histopathology
Purulent focus
Treatment
• Remove etiology
• Establish drainage
I. If Fluctuant: Incised with #15 blade and exudate expressed by digital pressure under LA.
II. If persist: Curette
• Irrigated with warm water and covered with moist gauge under light pressure.
•Patient asked to rinse with warm water every 2 hours and reassessed after 24 hrs.
•Systemic antibiotic: If persistent& systemic symptoms
•Residual pocket: Further periodontal management
PERICORONITIS PERICORONITIS
An inflammatory process involving the soft tissue covering of the crown of a partially erupted tooth.
Clinical features
• Pericoronitis may be Acute Subacute Chronic
• Mostly occurs in mandibular third molar area.
• Operculum favors accumulation of food debris and bacteria.
• Exacerbated by trauma, occlusion or foreign body entrapment.
Clinical features • Red, swollen & tender suppurating lesion
• Radiating pain to (Ear, throat and floor of mouth).
• Foul taste.
• Swelling of cheek.
• Trismus.
• Lymphadenitis, fever, malaise, leucocytosis.
Spread of infection• Posteriorly : Oropharyngeal area
• Medially : Base of tongue
• Peritonsillar abscess formation, cellulitis, Ludwig’s angina.
• Extend submucosally and form a vestibular abscess and may discharge as intra oral sinus.
• May involve Buccal, submandibular, pterygomandibular and submassetric spaces.
• May involve submaxillary, posterior cervical, deep cervical & retropharyngeal L.N.
Spread of infection
Immediate extraction advocated to prevent seeding of infection into deeper spaces
-Johri A, Piecuch JF 2011
Diagnosis
• Based on history, clinical & radiographic examination.
• All pericoronal flaps should be viewed with suspicion.
• In some cases malignant lymphoma, Ewing’s sarcoma, squamous cell carcinoma have been initially diagnosed as pericoronitis.
Treatment
Factors affecting
• Severity of inflammation
• Systemic complication
• Decision of retaining involved tooth
Treatment
• Gently flushing the area with warm water to remove debris and exudates.
• Swabbing the area with antiseptic after elevating the flap from tooth with scaler. Underlying debris are removed, area is flushed with warm water.
• Evaluation of occlusion.
• Antibiotics & Analgesics if indicated.
• Decision made to retain tooth or not- likelihood to erupt in functional position.
• If retaining the tooth- operculectomy
I. Periodontal knives II. ElectrosurgeryIII. Radiosurgical loopsIV. Chemical (Caustic agents)
ERYTHEMA MULTIFORME
• Syndrome of multiple etiology
• Oral+cutaneous lesion (separately or together)
• GINGIVA: Diffuse inflammation
• Extra oral: Skin eruption
+ Conjunctivitis
+ Upper respiratory tract infection
Erythema multiforme Primary herpetic stomatitis
Etiology Unknown Specific viral etiology
Age Young adults Children
Sex Males Equal frequency
Course 2-6 weeks 7-10 days
Clinical features
Skin lesions present(Target/ Bull’s eye lesion)
Not seen
Intraoral Extensive vesiclesPseudomembrane after rupture
Less extensiveNo pseudomembrane
Primary Herpetic Gingivostomatitis
Recurrent apthous stomatitis
Etiology:) Specific viral etiology. Immunopathologic basis
History Contact with affected person
History of reoccurence of prodromal symptom of burning before onset of disease
Age Children & young adult
Course 7-10 days
Clinical picture-Intraoral
Vesicles preceded ulceration which are seen on mobile & attached mucosa
Round or ovoid ulcers seen on mobile mucosa
Extra-oral Fever & malaise Not seen
NUG Primary Herpetic Gingivostomatitis
Etiology: Host bacterial interaction (fusospirochetes)
Specific viral etiology.
Necrotizing condition. Diffuse erythemaVesicular eruption.
Punched out gingival margin; pseudomembrane that peels off leaving raw areas.
Vesicles rupture and leave slightly depressed oval or spherical ulcer.
Marginal gingiva affected; other oral tissues rarely affected.
Diffuse involvement of gingiva, may include buccal mucosa and lips.
Uncommon in children. More frequent in children.
No definite duration. Duration of 7 to 10 days.
No demonstrated immunity. An acute episode results in some degree of immunity.
Not contagion. Contagious.
NUG Diptheria Syphilis
Etiology Host bacterial interaction.
C.diptheriae. T.pallidum.
marginal gingiva.
Affects Rarely affects Rarely affects
Membrane removal
easy. Difficult Not detachable.
Painful Painful Less Minimal.
Site affected Marginal gingiva
Throat, fauces, tonsils Any part of mouth
Serological findings
normal. normal. Abnormal (VDRL, Kahn).
Immunity Not conferred. Conferred by attack. Not conferred.
Contagiousness. Doubtful Contagion. Only direct contact
Antibiotic therapy
Relieves symptoms.
Minimal effect. Excellent results.
Bullous lichen planus Primary herpetic gingivostomatitis
Etiology Unknown Viral
History Stress, malnutrition Recent acute infection, stress, contact with infected person
Age Adult > 6 years
Sex Female more Equal
CourseProlonged indefinite
course
7-10 days
Clinical feature- Intraoral
Large painful blister on tongue and cheek that rupture & undergo ulceration
Initially vesicles seen, later they rupture & leave slightly depressed oval ulcer
Extraoral Co-involvement of skin Not seen
Histology “Saw tooth” rete pegs Tzank cell & multinucleated giant cells & acantholysis
NUG Desquamative Gingivitis
Chronic Destructive Periodontal Disease
Bacterial complex shows fusosphirochetal complex.
Bacterial smear shows many epithelial cells and few bacteria.
Bacterial smears variable.
Marginal gingiva affected.
Diffuse involvement of marginal and attached gingiva.
Marginal gingiva affected.
Acute history. Chronic history. Chronic history.
Painful. May/may not be painful.
Painless if uncomplicated.
Pseudomembrane. Patchy desquamation
of gingival epithelium.
No desquamation but purulent material present from pockets.
Papillary and marginal necrotic lesions.
Papilla no necrosis. Papilla-no necrosis.
Affects adults of both sexes.
Affects adults most often women.
Generally adults.
Fetid odor. None. Some odor but not fetid.
CONCLUSION
Acute gingival infections occur for short
duration and can be diagnosed easily in
contrast to chronic diseases which is
frequently not obvious. Still there are chances
of incorrect diagnosis which can mislead us.
Cases in which they are associated with
underlying systemic pathology, the
identification of gingival infection can help us
to diagnose the underlying systemic illness.
REFERENCES
• Randal W. Rowland. Necrotizing Ulcerative Gingivitis. Ann Periodontol 1999;4:65-73.
• Genco RJ, Goldman HM, Cohen DW, eds. Contemporary Periodontics. St. Louis: The C.V. Mosby Company; 1990:459-465.
• Yoji Murayama et al. Acute necrotizing ulcerative gingivitis: risk factors involving host defense mechanisms. Periodontol 2000 1994;6:116-124.
•Carranza. Clinical Periodontology. Elsevier 8th,9th,10th edition.
•Shafer. Text Book of Oral Pathology. Elsevier 5th edition
•Burket’s. Oral medicine diagnosis and treatment. Elsevier 10th edition.
•Amir H Ajar. Acute Herpetic Gingivostomatitis in Adults: A Review of 13 Cases, including diagnosis and management. Journal de l’Association dentaire canadienne Avril 2002,68(4):247-251.
•Enwonwu CO, Philips RS, Savage KO. Inflammatory cytokine profile and circulating cortisol levels in malnourished children withnecrotizing ulcerative gingivitis. Eur Cytokine Netw. 2005 Sep;16(3):240-8
•Enwonwu CO, Falker WA, Idigbe EO. Oro-facial gangrene (noma/cancrum oris): pathogenetic mechanisms. Crit Rev Oral Biol. 2000;11(2):159-71
•Johri A, Piecuch JF 2011. Immediate extraction advocated to prevent seeding of infection into deeper spaces. Oral Maxillofac Surg Clin North Am. 2011 Nov;23(4):507-11
•Rose & Mealey. Periodontics: medicine, surgery and implants. Elsevier 2004.
•Jan Lindhe. Clinical periodontology and implant dentistry. 5th ed. Blackwell Munksgaard 2008.
•Eley and Manson. Periodontics. 5th edition. Wright publishers.