Acute Gingival Infections
Question 1. Discuss etiology, clinical features and management of acute necrotizing gingivitis.
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Discuss the etiology, histopathology, clinical features and management of necrotizing ulcerative gingivitis (NUG).
Or
Define necrotizing ulcerative gingivitis and describe its clinical and histopathological features. Describe treatment of acute necrotizing ulcerative gingivitis in detail.
Or
Write short note on management of acute necrotizing ulcerative gingivitis.
Answer. Acute necrotizing ulcerative gingivitis is a distinct and specific clinical entry which is associated with rapidly progressive ulceration, especially commencing at the tip of interdental papilla, spread along the gingival margins leading to acute destruction of the periodontal tissue.
ANUG is renamed as necrotizing ulcerative gingivitis. It is also known as trench mouth as it is prevalent in soldiers who are working in trenches at the time of world war I. As Vincent had first described the bacteria which are associated with these infections, so the disease is known as Vincent’s angina.
Acute necrotizing ulcerative gingivitis is a rapid onset, painful microbial disease of gingiva caused primarily by fusobacterium species, probably in combination with oral spirochetes.
Read And Learn More: Periodontics Question And Answers
Etiology
- This is a fusospirochetal infection which is caused by fusospirochetal complex. The complex consists of following bacteria: Treponema microdentium, intermediate spirochetes, vibrios, fusiform bacilli and filamentous organisms, borrelia species.
- F. nucleatum is the main organism which is present inside the oral cavity.
- Fusobacterium species are Gram negative, obligate, anaerobic and rod shaped organisms.
- Temporary establishment of specific anaerobic environment allow fusobacterium and normal oral spirochetes to multiply synergistically, causing the infection.
Local Predisposing Factors
- Pre-existing gingivitis: Deep periodontal pockets, pericoronal flaps are vulnerable areas for occurrence of disease because they offer favorable environment for proliferation of fusospirochetes.
- Injury to gingiva: These are areas of gingiva traumatized by opposing teeth in malocclusion, such as palatal surface behind maxillary incisors.
- Smoking:
- Direct toxic effect of tobacco on gingiva.
- Vascular or other changes induced by nicotine.
Systemic Predisposing Factors
- Nutritional deficiency: Poor diet has been reported as predisposing factor on necrotizing ulcerative gingivitis. Nutritional deficiencies such as vitamin B and C results in the ANUG.
- Debilitating disease: The disturbances are metallic intoxification, severe gastrointestinal disorders and blood dyscrasias such as anemia, leukemia and AIDS.
Psychosomatic Factors
According to Cohen-Cole et al the impact of negative life events may lead to the activation of hypothalamic pituitary adrenal axis. This result in elevation of serum and urine cortisol levels, which is associated with depression of lymphocytes and the PMN function may predispose to necrotizing ulcerative gingivitis.
Acute Necrotizing Gingivitis Clinical Features
Intraoral Signs
- Lesions are characterized by punched out, crater-like depressions at crest of interdental papilla, involving marginal gingiva and rarely attached gingiva.
- Craters are covered by the grayish pseudomembranous slough; which is demarcated from remaining of mucosa by pronounced linear erythema.
- The ulcerations of NUG are of two types, i.e. lateralul cerations and necrosis. Lateral ulceration involving the buccal wall of papillae, margins and possible attched gingiva. Deep ulceration involves the necrosis of tissue of embrasure giving rise to typical truncated papillae.
- Gingival hemorrhage or pronounced bleeding on slightest stimulation.
- Fetid odor and increased salivation.
Intraoral Symptoms
- Lesions are sensitive to touch.
- Patient complains of constant radiating, gnawing pain that is intensified by eating spicy or hot foods and chewing.
- Metallic foul taste is present.
Extraoral Signs and Symptoms
- In mild-to-moderate stages of disease local lymphadenopathy and slight elevation in temperature are common features.
- In severe cases, high fever, increased pulse rate, leukocytes, loss of appetite and general lassitude are common.
Histopathological Features
- Microscopically both epithelium and underlying connective tissue is involved.
- There is destruction of surface epithelium and is replaced by pseudomembranous mesh of firin, necrotic epithelial cells, polymorphonuclear neutrophils and various other microorganisms.
- Underlying connective tissue is hyperemic with engorged capillaries and dense infitration of inflmmatory infitrate consisting of polymorphonuclear neutrophils.
- Four zones are described by Listgarten, i.e.
- Zone 1: Bacterial zone: It is the most superfiial zone and has various bacteria along with spirochetes of small, medium and large size.
- Zone 2: Neutrophil rich zone: It have numerous leucocytes, i.e. neutrophil with bacteria consisting of spirochetes of various types.
- Zone 3: Necrotic zone: It consists of dead tissue cells, connective tissue fragments and various spirochetes
- Zone 4: Zone of spirochetal infitration: It has wellpreserved tissue which is infitrated by spirochetes of intermediate and large size without other organisms.
Acute Necrotizing Gingivitis Differential Diagnosis
- Syphilitic gingivitis: Rarely seen on gingiva and does not spread.
- Pemphigus: Detected histologically and is common in older patients. Generalized skin lesions are also detected.
- Streptococcal gingivostomatitis: Diffse erythema is seen on posterior areas of oral mucosa and necrosis is absent over gingiva.
- Candidal gingivostomatitis: Presence of white deposits which can be rubbed of leaving erythematous areas.
- Benign mucous pemphigoid: Erosion is present, no evidence of necrosis is seen and occur in old patients.
- Gonococcal stomatitis: Oral mucosa consists of a grey membrane which leaves a raw bleeding surface.
- Agranulocytosis: Blood picture is the evidence which shows the systemic disease. Lesion does not show inflammatory reaction as there is diminished immunity.
Acute Necrotizing Gingivitis Diagnosis
- Gingival pain, ulceration and bleeding are all the diagnostic features of necrotizing ulcerative gingivitis.
- Microscopic examination of biopsy specimen can be used to differentiate necrotizing ulcerative gingivitis from specific infections i.e. tuberculosis or from neoplastic disease.
- It is important to take history to determine the underlying predisposing factors responsible for the disease.
Acute Necrotizing Gingivitis Staging
According to Pindborg and Colleagues
They describe following stages in progression of necrotizing ulcerative gingivitis
- Stage 1: Only the tip of inter – dental papilla is affcted.
- Stage 2: Lesion extends to marginal gingiva and causes punched – out papilla.
- Stage 3: Attached gingiva is also affected.
- Stage 4: Bone is exposed.
According to Horning and Cohen
They extend the staging of oral necrotizing diseases as:
- Stage 1: Necrosis of the tip of interdental papilla. (NUG)
- Stage 2: Necrosis of the entire papilla. (Either NUG or NUP)
- Stage 3: Necrosis extending to gingival margin. (NUP)
- Stage 4: Necrosis extending also to attched gingiva. (NUP)
- Stage 5: Necrosis extending into buccal or labial mucosa. (Necrotizing stomatitis)
- Stage 6: Necrosis exposing alveolar bone. (Necrotizing stomatitis)
- Stage 7: Necrosis perforating skin of cheek. (NOMA)
Acute Necrotizing Gingivitis Treatment
Treatment of necrotizing ulcerative gingivitis consists of
- Alleviation of acute inflammation by reduction of the microbial load and removal of necrotic tissue
- Treatment of chronic disease either underlying the acute involvement or elsewhere in the oral cavity
- Alleviation of generalized symptoms such as fever and malaise.
- Correction of systemic conditions or factors that contribute to the initiation or progression of gingival changes.
- Treatment of necrotizing ulcerative gingivitis follows a sequence which consists of three clinical visits i.e.
First Visit
- Primary goal is the treat of an acute lesion.
- Patient should be evaluated completely regarding the medical history as well as history of recent illness.
- Dietary history, history of smoking, risk factors for HIV and psychological factors are evaluated.
- Perform general examination to examine the vital signs and palpate the lymph nodes, mainly submaxillary and submental lymph nodes. Examine the patient for skin lesions.
- Remove pseudo – membrane and the non attched surface debris by moist cottn swab and apply topical anesthetic agent over the affected area.
- Supragingival scaling with ultrasonic instruments can be performed.
- Avoid subgingival scaling and curettage as this can cause extension of infection and lead to bacteremia.
- Four weeks time is needed to get symptom free. Both periodontal surgery and extractions are postponed till patient get symptom free.
- Following antibiotic regimen should be given to the patient:
- Amoxicillin 500mg orally every 6 hours for 10 days.
- If patient is allergic to amoxicillin, erythromycin 500mg every 6 hourly or metronidazole 500 mg twice daily for a week.
- For controlling pain, an analgesic such as non-steroidal inflammatory drug can be prescribed.
Following Instructions Should be Given to Patient
- Avoid tobacco, alcohol, and condiments.
- Rinse with a glassful of an equal mixture of 3% hydrogen peroxide and warm water every 2 hours and/or 0.12% chlorhexidine solution twice daily.
- Patient should be asked to take adequate rest. Pursue usual activities, but avoid excessive physical exertion.
- Toothbrushing should be confied to removal of surface debris with either a bland dentifrice or just water and an ultrasof brush; overzealous brushing and the use of dental floss or interdental cleaners will be painful. Chlorhexidine mouth rinses are helpful in controlling biofim in the oral cavity.
- An analgesic, such as a non steroidal anti-inflammatory drug (NSAID), is appropriate for pain relief.
- Patients with systemic complications i.e. high fever, malaise, anorexia, or general debility should be given antibiotics and instructed to get plenty of bed rest and drink lots of fluids.
Second Visit
- This visit is scheduled 1 or 2 days after the first visit.
- Check the patient for resolution of systemic signs and symptoms.
- Lesional area will be erythematous, but with the marked reduction in necrotic tissue, scaling can be performed.
- Patient is asked to follow same instructions which are given in the first visit.
Third Visit
- Following 5 days after the second visit, evaluate the patient for resolution of symptoms and a complete protocol for periodontal management is planned.
- Ask the patient to discontinue hydrogen peroxide rinse and continue with chlorhexidine mouthwash for 2 to 3 weeks.
- If needed, scaling and root planning is repeated. Patient should be reinstructed to follow appropriate plaque control measures.
- For preventing possible recurrence. Patient is counseled on nutrition, smoking cessation and other associated habits.
- Schedule the appointment for treatment of chronic gingivitis, periodontal pockets and for the elimination of all local irritants including the defective restorations.
- Re-evaluate the patient after one month for maintenance of oral hygiene, health habits, psychosocial factors and determination of need for reconstructive or aesthetic surgery.
Additional Treatment Considerations
It consists of:
- Contouring of gingival margin
- Nutritional supplements
Contouring of Gingival Margin
In necrotizing ulcerative gingivitis as there is severe loss of interdental gingiva as well as bone, the normal gingival architecture is restored by periodontal plastic surgery or reshaping the gingiva surgically.
Nutritional Supplements
- As patient is unable to take the food because of pain, nutritional supplements can be indicated along with the local treatment.
- Provide standard multivitamin preparation along with therapeutic dose of vitamin B and C.
Question 2. Describe clinical features and management of acute necrotizing ulcerative gingivitis. How would you differentiate it from other similar lesions?
Answer.
Difference between Necrotizing Ulcerative Gingivitis and Primary Herpetic Gingivostomatitis
Difference between ANUG and Aphthous Stomatitis
Question 3. Write short note on herpetic gingivostomatitis.
Or
Discuss acute herpetic gingivostomatitis.
Answer. It is the viral infection caused by herpes simplex virus. It occurs in infants and children younger than 6 years of age but is also seen in adults.
Primary infection with herpes simplex virus in the oral cavity results in a condition known as acute herpetic gingivostomatitis, which is an oral infection that is often accompanied by systemic signs and symptoms.
Herpetic Gingivostomatitis Clinical Features
- It develops mostly in children and young adults.
- Both males and females are equally affected.
- There is development of painful vesicular lesions on all the mucosal surfaces which rupture to produce foul smelling ulcers.
- Patient become febrile, drools and has signifiant malaise and have tender cervical lymphadenopathy.
- Lesions and acute illness last for 10 days and resolve with scar formation.
- HSV-1 gain access to patient via direct or airborne water droplet transmission from the infected individual.
- Clinical course is limited by synthesis of viral specifi antibodies.
- After the primary infection, virus ascends through sensoryand the autonomic nerves and persists as latent herpes simplex virus in neuronal ganglia which innervates the site.
- HSV-1 resides inside the trigeminal ganglion.
Oral Signs
- It appears as diffuse, shiny erythematous, involvement of gingiva and adjacent oral mucosa with varying degree of edema and gingival bleeding.
- In its initial stage, it appears as discrete, spherical, gray vesicles dispersed in different areas, e.g. labial and buccal mucosa, sof palate, pharynx and tongue. After approximately 24 hours the vessels rupture and form painful ulcers with a red, elevated, halo-like margins and a depressed yellow and grayish white central portion.
- Diffuse, edematous, erythematous enlargement of gingiva with tendency towards bleeding is seen.
Oral Symptoms
- Generalized soreness of oral cavity which interferes with eating and drinking.
- The ruptured vesicles are sensitive to touch, thermal changes and foods.
Herpetic Gingivostomatitis Diagnosis
It is established from patients history and clinical findings. For confimatory tests, the material may be obtained from the lesion and submittd to laboratory.
- Direct smear: Material is obtained from the base of lesion and smeared and stained. The finding of multinucleated cells with swelling, ballooning and regeneration is adequate for diagnosis.
- Inoculation of virus from suspected site, to tissue culture.
Herpetic Gingivostomatitis Differential Diagnosis
- Herpangina: Group A coxsackie virus leads to herpangina. Lesions in herpes simplex are located predominantly in anterior region of mouth while of herpangina are seen in posterior oral pharynx. Duration of illness is longer with herpes simplex.
- Erythema multiforme: Vesicles in erythema multiforme are more extensive as compared to primary herpetic gingivostomatitis and on rupture they show pseudomembrane formation.
- Stevens-Johnson syndrome: It is characterized by vesicular hemorrhagic lesions in oral cavity, hemorrhagic ocular lesions and bullous skin lesions.
- Bullous lichen planus: It is characterized by formation of large blisters on tongue and cheek which rupture and undergo ulceration; it undergoes a prolonged and indefinite course.
- Apthous ulcer: It is manifested as as single ulcer with erythematous halo which surround yellow firinopurulent membrane.
Herpetic Gingivostomatitis Management
Various medications are used, i.e.
Local Application
- Using 8% zinc chloride, Talbot’s iodine, phenol, riboflavin, thiamine, etc.
- Chlortetracycline has been successfully used as mouthwash, applied topically in 3% ointment or administered systemically in form of 250 mg capsules.
Palliative Treatment
- Make the patient comfortable until the disease runs its course, i.e. 7 to 10 days
- Plaque, food debris, calculus are removed to reduce gingival inflammation
- Relief in pain is obtained with dyclonine hydrochloride—a topical anesthetic mouthwash.
Supportive Treatment
Copious fluid intake and antiviral therapy for management of toxic systemic complications. For relief of pain, systemically administration is usually suffient.
Question 4. Write short note on pericoronitis.
Or
Write short note on acute pericoronitis.
Or
Discuss pericoronitis in detail.
Answer. The term pericoronitis refers to inflammation of gingiva in relation to crown of an incompletely erupted tooth.
It occurs more frequently in mandibular third molar area.
Pericoronitis Clinical Features
- The partially erupted or impacted mandibular third molar is the most common site for pericoronitis.
- The resultant clinical picture consists of markedly red, edematous suppurating lesion that is extremely tender with radiating pain to ear, throat and flor of mouth.
- Patient is uncomfortable because of foul taste and inability to close jaws.
- In addition to pain, swelling of cheek in region of angle of jaw is seen.
- Lymphadenitis can be present.
- Toxic symptomatic symptoms such as fever, malaise and leukocytosis are also present.
Pericoronitis Treatment
The treatment of pericoronitis depends on:
- Severity of inflammation.
- The systemic complication.
- The advisability of retaining involved tooth.
First Visit
- Area is gently flushed with warm water to remove superficial debris and exudates followed by application of topical anesthetic solution.
- Marginal gingiva is reflcted with scalar and underlying debris is, also removed and area is flshed with warm water.
- Instructions to patient include hourly rinses with solution of tea spoonful of salt in a glass of lukewarm water, rest, copious fluid intake and administration of systemic antibiotics, if toxic symptoms are present.
- If the gingival flap is swollen and fluctuant an anteroposterior incision to establish drainage is made with No. 15 blade, followed by insertion of ¼th inch gauze.
Second Visit
- In the next visit, determination is made as to whether the tooth is to be retained or extracted. If it is decided to retain the tooth, the necessary surgical procedures are performed using a periodontal knife or electrosurgery. Under anesthesia, a wedge-shaped incision is made to section a tissue that includes gingival flp with tissue distal to the involved tooth as well.
- After tissue is removed, a periodontal pack is placed.
Pericoronitis Complications
- The involvement may become localized in form of pericoronal abscess.
- It occurs in partly erupted vital tooth, it may give rise to cyst formation.
- It may spread posteriorly into the oropharyngeal area and medially into base of tongue, making it difficult for patient to swallow.
- Depending on severity, there is involvement of submaxillary, cervical, deep cervical and retropharyngeal lymph nodes.
- Peritonsillar abscess formation, cellulitis and Ludwig’s angina are infrequent but nevertheless potential sequelae of pericoronitis.
Question 5. Write short note on acute gingival infections.
Or
Write short note on acute gingival lesions.
Answer. Following are the acute gingival infections:
Classification According to Manson
- Traumatic lesions of gingiva:
- Physical injury
- Chemical injury
- Viral infections:
- Acute herpetic gingivostomatitis
- Herpangina
- Hand foot and mouth disease
- Measles
- Herpes varicella/zoster virus infections
- Glandular fever.
- Bacterial Infections:
- Necrotizing ulcerative gingivitis.
- Tuberculosis.
- Syphilis.
- Fungal Disease: Candidiasis.
- Gingival abscess.
- Aphthous ulceration.
- Erythema multiforme.
- Drug allergy and contact hypersensitivity.
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