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ACUTE GINGIVAL INFECTION
Sudden onset of a condition
Relating to the gums
Infection Pathological state resulting from the invasion of the body by pathogenic microorganisms
ACUTE GINGIVAL INFECTION Infection or lesion Affect gingiva Sudden onset Limited duration Well defined clinical features .
1) Traumatic lesions-physical and chemical 2) 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 abscess 6) Aphthous ulceration 7) Pericoronitits 8) Erythema multiforme 9) Drug allergy and contact hypersensitivity .
ACUTE HERPETIC GINGIVOSTOMATITIS .
• Contagious. • Ectodermal structures. • No sex predilection.• Caused by herpes simplex virus type 1 (HSV-1). • Age-below 6 years.Affected. .
Latency of herpes simplex virus .
erythematous. • 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. shiny involvement of gingiva and adjacent oral mucosa. • Edema and gingival bleeding.Oral signs • Diffuse.
. • Ruptured vesicles : Painful and sensitive to touch. fruit juices and coarse food. • Infants: Irritability and refusal to take food.Oral symptoms • Soreness. thermal changes.
105º F) • Malaise • Headache .Extra oral signs and symptoms • Cervical adenitis • Fever (101º F.
Surface is covered by exudate Fibrin. PMN and degenerated cells . Tzanck cells. Connective tissue : Inflammatory cells. When vesicles rupture . Ballooning degeneration of cells.Histopathology • • • • • • Intraepithelial blister. Lipschütz bodies.
Diagnosis • Patient history and clinical findings. • Immunofluorescent staining of smears. . • Direct smear finding • Viral isolation and identification. • DNA hybridization.
• 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.
• 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. • Local or systemic antibiotics to prevent secondary infection. • Nutritional supplements. • Topical anesthetics before eating. • NSAID (Fever and pain).
22) Anterior faucial walls (causes ulceration & sore throat) Heals in 7-10 days Rarely affects gingiva HAND.HERPANGINA • • • Coxsackie A(1-6. 5 or 6) Oral vesicles > small ulcers Heals in 10-14 days . FOOT AND MOUTH DISEASE • • • Coxsacke A (16 .10.16.8.
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 .
R. S.Challacombe. J.J. seen through out the world • West Africa + Western & Southern India • Both direct and indirect effects on oral mucosal immunity Affect both cellular and humoral immunity & both specific and innate immunity.Naglik (2006) .Caused by HIV or Human Immunodeficiency virus HIV 1 HIV 2 Most common.
C1. C2 are AIDS . B3.1993 CDC CLASSIFICATION CD4 count Asymptomatic (/c mm) >500 200-499 <200 A1 A2 A3 Symptomatic AIDS indicator condition C1 C2 C3 B1 B3 B3 A3. C3.
. vascular neoplasm • • • Malignant tumor ( localized & slowly growing lesion ) Etiology: Activation of the latent HHV-8 In HIV + ve : converts the diagnosis into AIDS.GINGIVAL LESIONS KAPOSI’S SARCOMA • Rare . multifocal .
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. 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. that often extends into attached gingiva.
Bacterial infections • • • Acute necrotizing ulcerative gingivitis Tuberculosis Syphilis .
noncommunicable. gingival infection of complex etiology .NECROTIZING ULCERATIVE GINGIVITIS A rapidly destructive.
HISTORY 400 B. Historical war of Xenophon’s troop st Roman Army: 1 Greek Century A.D Soldiers of the army .C.
SYNONYMS • Acute ulceromembraneous gingivitis • Trench mouth • Cheilokake • Phagedenic gingivitis • Ulcerative gingivitis • Vincent’s stomatitis • Plant-Vincent’s stomatitis .
SYNONYMS •Stomatitis ulcerosa •Fusospirillary gingivitis •Fetid stomatitis •Putrid stomatitis •Acute septic gingivitis •Pseudomembranous angina •Spirochetal stomatitis .
CLASSIFICATION • Acute disease • Subacute disease • Recurrent disease • Chronic disease .
PATIENT HISTORY • Sudden in onset • Following debilitating disease or acute respiratory tract infection. poor nutrition. • Change in living habits • Inadequate rest. . stress. tobacco use.
Crest of interdental papilla .Covered by gray pseudomembrane.Spontaneous or slight provocation. • Gingival hemorrhage .ORAL SIGN • Punched out craters . • Linear erythema. .
•No pocket . •Increased salivation.•Fetid odor. •Can occur in disease free mouth or superimposed on chronic gingivitis.
ORAL SYMPTOMS • Lesions are sensitive to touch • Constant radiating. gnawing pain • Metallic foul taste in the mouth • Pasty saliva .
• Loss of appetite. • Leukocytosis. • Elevated temperature.EXTRA ORAL SIGNS AND SYMPTOMS • Local lymphadenopathy. . • Increased pulse rate.
headache.EXTRA ORAL SIGNS AND SYMPTOMS •GeneraL lassitude. •Head ache & mental depression . •GIT disorder. constipation. •Insomnia. mental depression.
CLINICAL COURSE NECROTIZING ULCERATIVE GINGIVITIS NECROTIZING ULCERATIVE PERIODONTITIS SYSTEMIC COM PLICATION .
STAGING OF ANUG Pindborg et al 1966 1. Attached gingiva affected. Erosion at tip of the interdental papilla. 3. Marginal gingiva involved (punched out papilla). . 4. 2. 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 .
Necrotizing stomatitis Stage 7: necrosis perforating skin of cheek (0%) .NUP Stage 5: necrosis extending into buccal or labial mucosa (6%).NOMA .Necrotizing stomatitis Stage 6: necrosis exposing alveolar bone (1%) .STAGING OF ANUG Stage 4: necrosis extending to the attached gingiva (1%).
necrotic epithelial cells. • Cells : Hydropic degeneration .HISTOPATHOLOGY • Epithelium : :Destroyed : Replaced by meshwork of fibrin. PMNs and microorganisms.
.•Connective tissue : : Hyperemic : Engorged blood vessels : Dense infiltration of PMNs : Numerous plasma cells at the periphery.
Fusiform bacillus: Borrelia vincentii: •Gm -ve spirochete •3–6 long loose spirals •10-15 µm in length •Motile organism • • • • Gm +ve anaerobe rod 5.14 µm in length 0.ETIOLOGY • Plaut 1894 and Vincent 1896 .0 µm in diameter Non motile .fusiform bacillus and spirochetes.5 -1.
•Chung et al 1983 : Higher IgG and IgM levels to intermediate sized spirochetes and P.•Loesche et al 1982: Constant flora : P. intermedia.intermedia . Fusobacterium. Treponema & Selenomonas Variable flora : Heterogeneous bacteria.
(Courtois 1983) .Relation of bacteria to the characteristic lesion Listgarten 1965 • • • • Zone 1: Zone 2: Zone 3: Zone 4: Bacterial zone Neutrophil rich zone Necrotic zone Spirochetal infiltration Cocci and rods in addition to the spirochetes within the adjacent non-necrotic connective tissue region was found.
(Cogen et al 1983) • CD4:CD8 ratio is inversed.ROLE OF HOST RESPONSE • Depression in PMN chemotaxis and phagocytosis. (Enwonwu 1994) • Dysregulated cytokine production (Enwonwu et al 2005) .
Local factors Preexisting gingivitis Injury to gingiva Smoking 2. Systemic factors Nutritional deficiencies Debilitating disease 3. Psychosomatic factors .Predisposing factors 1.
Humoral antibody: high serum IgG or IgM levels to spirochetes and P. HIV infection Altered immune systems Chung et al Cogen et al Claffey et al Cogen et al. . Smoking Cohen-Cole et al Kowolik & Nesbet Clarke et al Johnson & Engel Melnick et al.References Predisposing factors Emotional Cohen-Cole et al stress Schoor & Havrilla Johnson & Engel Melnick et al. Pathogenesis Increased steroid levels depress immune defense systems. SLE. Systemic Ryan et al diseases Deasy et al Jaworsky et al.intermedia. Nicotine exposure initiates vasoconstriction resulting in relative ischemia contribute to tissue destruction. Cell mediated immnity: Depressed Neutrophil & Lymphocyte activitylow CD4+/CD8+ ratio due to high CD8+ level. Cancer (immunosuppression) Von Willebrands disease (coagulation disorder.
Pindborg JJ.Prevalence • Occurs at all age with highest incidence b/w 2030 yrs (Dean 1945). • Common in children with Down syndrome than in other mentally retarded children. • Common in children from low SES in underdeveloped countries. Devnath KR in 1966 concluded that 58% of the patients were younger than 10 yrs. • In India. Bhat M. .
King 1943 .Communicability • Disease associated with the fusospirochetal bacterial complex is transmissible but has not been shown to be communicable or contagious.
.Diagnosis • Gingival pain • Ulceration • Bleeding • Important to identify the underlying predisposing factors.
. • No fetid odor. Agranulocytosis • No inflammation. Vincent’s angina • Fuso-spirochetal infection of oropharynx and throat. • Blood investigation can differentiate from NUG.DIFFERENTIAL DIAGNOSIS Streptococcal gingivostomatitis • Diffuse erythema. • No necrosis.
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) .
12% CHX mouthwash. .Instructions to the patient • Avoid- • Mouth rinse: : 1:1 3% H2O2 and warm water 2 hourly or 0.
3%Hydrogen peroxide ( 50 % dilution in warm non irritating solution) Mechanism of action: 1. Effervescence action: : Mechanical cleansing (Nascent oxygen bubbles going away) : Highly significant .
Oxidative prperty: H2O2 Catalase & Peroxidase H2O+0 [Nascent oxygen] Bactericidal Anaerobic bacteria Other reactive oxygen species produced: superoxide and hydroxyl radical (More powerful) (Davidson and Branen.2. 1993) .
.Second visit (1 to 2 days later) • Evaluate patient for signs and symptoms.Scaling is done • Shrinkage of gingiva.May expose previously covered calculus – Remove gently. • If sensitivity permits. • Gingival margins : Erythematous but without superficial pseudomembrane.
• OHI reinforced.Third visit (5 days later) • Patient should be symptom free. • Scaling and root planing are repeated. . • H2O2 mouthwash is discontinued. but CHX rinses can be maintained for 2-3 weeks. • Patient counseling.
Subsequent visits • Tooth surfaces in the involved areas are scaled and smoothened. • Further periodontal therapy if required • Patient should be reevaluated at 1 month .
A and B complex.Additional treatment considerations • Gingival contouring • Antimicrobials therapy • Supportive systemic treatment • Nutritional supplements.vit C. .
Persistent or recurrent cases • Reassessment of differential diagnosis • Underlying systemic disease causing immunosuppression • Inadequate local therapy • Inadequate compliance .
running horse gangrene) • • • • • • • Fusospirochetal meningigits Peritonitis Pulmonary infections Toxemia Brain abscess Necrotizing stomatitis Recurrent infection . gangrenous stomatitis.SEQUELAE OF INADEQUATE TREATMENT • NOMA (Cancrum Oris.
TUBERCULOSIS: • specific granulomatous infectious disease • • • extremely rare and forgotten entity Gingival lesion: Secondary to primary tuberculosis Lesion: Nodules. Deep ulcers. or Elevated fissures .
Snail track ulcers : Vesiculobulous lesions • Tertiary: Gumma (rarely) .SYPHILIS • • Primary: Ulcer Secondary (More common) : Mucous patches.
Chronic atrophic candidiasis 4. Acute atrophic candidiasis 3.FUNGAL INFECTION 1. Oro-pharyngeal candidiasis . Acute pseudomembranous candidiasis 2.
ACUTE GINGIVAL ABSCESS .
Abscess confined to the gingiva May discharge spontaneously Spread into underlying tissue Periodontal abscess .
rapidly expanding lesion with sudden onset.red swelling with shiny surface. • Limited to marginal and interdental papilla. .Clinical features • Localized. painful. • Initially.
Ruptures spontaneously. .• • • Fluctuant and pointed with a surface orifice (24-48 hrs) Adjacent teeth sensitive to percussion.
Etiology • Forceful impaction of foreign substance into gingiva. • Trauma. . • Bacteria carried deep into tissues.
Histopathology Epithelium : Intra and extracellular edema. leukocytes invasion and ulceration. Edematous tissue with vascular engorgement PMNs Purulent focus .
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.Treatment • Remove etiology • Establish drainage I.
•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 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. Exacerbated by trauma. occlusion or foreign body entrapment. Operculum favors accumulation of food debris and bacteria.
• Swelling of cheek. throat and floor of mouth). fever. • Lymphadenitis. • Foul taste. . • Trismus. swollen & tender suppurating lesion • Radiating pain to (Ear. malaise. leucocytosis.Clinical features • Red.
cellulitis.Spread of infection • Posteriorly : Oropharyngeal area • Medially : Base of tongue • Peritonsillar abscess formation. . • Extend submucosally and form a vestibular abscess and may discharge as intra oral sinus. Ludwig’s angina.
deep cervical & retropharyngeal L. Immediate extraction advocated to prevent seeding of infection into deeper spaces -Johri A. pterygomandibular and submassetric spaces. Piecuch JF 2011 . submandibular. May involve submaxillary.N.Spread of infection • • May involve Buccal. posterior cervical.
• 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.
• • • Severity of inflammation Systemic complication Decision of retaining involved tooth
• 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.
Periodontal knives II.operculectomy I. Electrosurgery III. • If retaining the tooth. Chemical (Caustic agents) .Radiosurgical loops IV.• Decision made to retain tooth or notlikelihood to erupt in functional position.
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 Etiology Unknown Primary herpetic stomatitis Specific viral etiology Age Sex Course Clinical features Intraoral Young adults Males 2-6 weeks Skin lesions present (Target/ Bull’s eye lesion) Extensive vesicles Pseudomembrane after rupture Children Equal frequency 7-10 days Not seen Less extensive No pseudomembrane .
Vesicles preceded ulceration Intraoral which are seen on mobile & attached mucosa Extra-oral Fever & malaise .Primary Herpetic Gingivostomatitis Etiology:) Specific viral etiology. Recurrent apthous stomatitis Immunopathologic basis History Contact with affected person History of reoccurence of prodromal symptom of burning before onset of disease Age Course Children & young adult 7-10 days Round or ovoid ulcers seen on mobile mucosa Not seen Clinical picture.
Marginal gingiva affected. Vesicles rupture and leave slightly depressed oval or spherical ulcer. Duration of 7 to 10 days. No definite duration. An acute episode results in some degree of immunity. Diffuse erythema Vesicular eruption.NUG Etiology: Host bacterial interaction (fusospirochetes) Necrotizing condition. Diffuse involvement of gingiva. Uncommon in children. Punched out gingival margin. More frequent in children. other oral tissues rarely affected. . may include buccal mucosa and lips. No demonstrated immunity. Primary Herpetic Gingivostomatitis Specific viral etiology. Not contagion. pseudomembrane that peels off leaving raw areas. Contagious.
Any part of mouth Abnormal (VDRL. Not conferred. .pallidum.diptheriae. Host bacterial interaction. Not conferred. Rarely affects Membrane removal Painful Site affected Serological findings Immunity Contagiousness. Rarely affects Syphilis T. Minimal. Affects Diptheria C.NUG Etiology marginal gingiva. tonsils normal. easy. Contagion. Not detachable. Kahn). Excellent results. Only direct contact Antibiotic therapy Relieves symptoms. fauces. Painful Marginal gingiva normal. Doubtful Difficult Less Throat. Minimal effect. Conferred by attack.
Bullous lichen planus Etiology History Age Unknown Stress. later tongue and cheek that they rupture & leave slightly rupture & undergo ulceration depressed oval ulcer Co-involvement of skin “Saw tooth” rete pegs Not seen Tzank cell & multinucleated giant cells & acantholysis . malnutrition Adult Viral Primary herpetic gingivostomatitis Recent acute infection. stress. contact with infected person > 6 years Sex Course Clinical featureIntraoral Extraoral Histology Female more Prolonged indefinite course Equal 7-10 days Large painful blister on Initially vesicles seen.
None. Some odor but not fetid. Patchy desquamation of Chronic Destructive Periodontal Disease Bacterial smears variable. Papilla no necrosis. Affects adults of both Affects adults most sexes. Desquamative Gingivitis Bacterial smear shows many epithelial cells and few bacteria. Papillary and marginal necrotic lesions. often women. Chronic history. Diffuse involvement of marginal and attached gingiva. gingival epithelium. Acute history. Chronic history. Painful. Pseudomembrane. . Generally adults. Fetid odor. Marginal gingiva affected. May/may not be painful. Papilla-no necrosis. Painless if uncomplicated.NUG Bacterial complex shows fusosphirochetal complex. No desquamation but purulent material present from pockets. Marginal gingiva affected.
Still there are chances of incorrect diagnosis which can mislead us.CONCLUSION Acute gingival infections occur for short duration and can be diagnosed easily in contrast to chronic diseases which is frequently not obvious. . the identification of gingival infection can help us to diagnose the underlying systemic illness. Cases in which they are associated with underlying systemic pathology.
Periodontol 2000 1994. eds. 1990:459-465. Necrotizing Ulcerative Gingivitis. Goldman HM.4:65-73. . Rowland.V. Ann Periodontol 1999. Acute necrotizing ulcerative gingivitis: risk factors involving host defense mechanisms. Cohen DW. Contemporary Periodontics. Louis: The C. Mosby Company.6:116-124. • Genco RJ. St.REFERENCES • Randal W. • Yoji Murayama et al.
9th. •Amir H Ajar.10th edition. Elsevier 10th edition. •Shafer. Elsevier 5th edition •Burket’s. Oral medicine diagnosis and treatment. Clinical Periodontology. Elsevier 8th. including diagnosis and management. Journal de l’Association dentaire canadienne Avril 2002. Acute Herpetic Gingivostomatitis in Adults: A Review of 13 Cases. .68(4):247-251. Text Book of Oral Pathology.•Carranza.
Eur Cytokine Netw.11(2):159-71 •Johri A. Falker WA. 2000. Inflammatory cytokine profile and circulating cortisol levels in malnourished children withnecrotizing ulcerative gingivitis. 2005 Sep.16(3):240-8 •Enwonwu CO. Idigbe EO.•Enwonwu CO. Savage KO. Crit Rev Oral Biol. Immediate extraction advocated to prevent seeding of infection into deeper spaces. Philips RS. Piecuch JF 2011. Oro-facial gangrene (noma/cancrum oris): pathogenetic mechanisms. Oral Maxillofac Surg Clin North Am.23(4):507-11 . 2011 Nov.
5th edition. Clinical periodontology and implant dentistry. •Jan Lindhe.•Rose & Mealey. Elsevier 2004. Blackwell Munksgaard 2008. Periodontics: medicine. 5th ed. Wright publishers. . •Eley and Manson. surgery and implants. Periodontics.
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