Acute Gingival Infections

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.