Necrotizing Ulcerative Gingivitis

Necrotizing ulcerative gingivitis can be defined as an acute , and sometimes recurring gingival infection of complex etiology . Characterized by rapid onset of gingival pain, interdental gingival necrosis , and bleeding .

Necrotizing ulcerative gingivitis has been called many names: -Vincents disease - Trench mouth -Acute necrotizing ulcerative gingivitis - Fusospirochetal gingivitis

The patients affected are typically adolescents or young adults, may be cigarettes smokers, and are often psychologically stressed.

During world II up to 14% of the 14% Danish military personnel encountered NPD. Also civilians suffered from the disease

After world war II the prevalence of NPD declined substantially and in industrialized countries NPD it is now rare

Clinical signs NUG

Pain Ulceration Necrosis of the interdental papillae Bleeding either spontaneous or to gentle manipulation.

Necrotizing gingivitis is an inflammatory destructive gingival condition , characterized by ulcerated and necrotic papillae and gingival margins resulting in a characteristic punched out appearance

The ulcers are covered by a yellowish white or grayish slough which is termed Pseudo membrane

The sloughed material has no coherence , and bears little resemblance to a membrane. It consists primarily of fibrin and necrotic tissue with Leucocytes, erythrocytes and masses of bacteria

Removing of the sloughed material results bleeding and ulcerated underlying tissue becomes exposed

The necrotizing lesions develop rapidly and are painful , but in the initial stages , when the necrotic areas are relatively few and small , pain is usually moderate. Severe pain is often the chief reason for the patient to seek treatment

Bleeding is readily provoked . And may start spontaneously as well as in response to even gentle touch.

In early phases of the disease lesions are typically confined to the top of a few interdental papillae

The first lesions are often seen interproximally in the mandibular anterior region . But they may occur in any interproximal space

In regions where lesions first appear , there are usually also signs of preexisting chronic gingivitis , but the papillae are not always edematous at this stage .

The zone between the marginal necrosis and the relatively unaffected gingiva usually exhibits a well demarcated narrow erythematous zone

This is an expression of hyperemia due to dilation of the vessels in the gingival connective tissue in the periphery of the necrotic lesions

Acute necrotizing ulcerative gingivitis; typical lesions with progressive tissue destruction

Acute necrotizing ulcerative gingivitis: typical lesions with spontaneous hemorrhage

Acute necrotizing ulcerative gingivitis: typical lesions have produced irregular gingival contour.

Involvement of Alveolar Mucosa

When the necrotic progresses beyond the mucogingival junction the condition is donated Necrotizing Stomatitis (NS) The disease is related to compromised immune functions , and malnutrition

Differential diagnosis of NUG is that from primary herpetic gingivostomatitis

Differential Diagnosis
NUG Etiology: Bacteria Age: 15-30 years Site: Interdental papillae Symptoms: Ulceration and necrotic tissue and a yellowish-white Duration:1-2 days if treated Contagious: No Immunity: No Healing: Destruction of periodontal tissue remain. PHGS Etiology: Herpes simplex virus Age : Frequently children Site: Gingiva and entire mucosa Symptoms: Multiple vesicles which burst leaving small round fibrin-covered ulcers which tend to coalesce. Duration: 1-2 weeks Contagious: Yes Immunity: Partial Healing: No permanent destruction

AHGS

Swelling of Lymph Nodes

Swelling of regional lymph nodes may occur in NPD is particularly evident in advanced cases. Such symptoms are usually confined to the submandibular lymph nodes , but the cervical lymph nodes may also be involved. In children with NPD , swelling of lymph nodes and increased bleeding tendency are often the most pronounced clinical findings

Fever and Malaise

Fever and malaise is not a consistent characteristic of NPD. Some investigations indicate that elevated body temperature is not common in NG and when present the elevation of body temperature is usually moderate. The disagreement on this point may , in fact be due to misdiagnosis of primary herpetic gingivostomatitis

Histopathology
Necrotizing gingivitis are characterized by ulceration with necrosis of epithelium and superficial layers of the connective tissue An important aspect is the role of the microorganisms in the lesion , because they have been demonstrated not only in the necrotic tissue components but also in vital epithelium and connective tissue

The surface cover of yellowish white or grayish slough the tissue is infiltrated by large and medium sized spirochetes , but no other microorganisms have been seen

In the vital connective tissue the vessels are dilated. They also proliferate to form granulation tissue , and the tissue is heavily infiltrated by leucocytes. In acute processes the inflammatory infiltrate is dominated by Neutrophils , in the deeper tissue the inflammatory process comprises large numbers of monocytes and plasma cells

Oral Hygiene
The oral hygiene in patients with NPD is usually poor . Moreover , brushing of teeth and contact with the acutely inflamed gingiva is painful . Therefore , large amounts of plaque on the teeth are common , especially along the gingival margin . A thin , whitish film sometimes covers parts of the attached gingiva. This film is a characteristic finding in patients who have neither eaten nor performed oral hygiene for days, it is composed of desquamated epithelial cells and bacteria , it is easily removable

Treatment
The treatment of the necrotizing periodontal diseases is divided into two phases : Acute Maintenance

Acute Phase Treatment

The aim of the acute phase treatment is to eliminate disease activity as manifest by ongoing tissue necrosis developing laterally and apically. A further aim is to avoid pain and general discomfort which may severely compromise food intake

The first consultation scaling should be attempted as thorough as the condition allows. Ultrasonic scaling may be preferable, with minimal pressure against the soft tissues , ultrasonic cleaning may accomplish the removal of soft and mineralized deposits

Patients should be instructed in substituting tooth brushing with chemical plaque control in such areas until healing is accomplished

Hydrogen peroxide and other oxygen releasing agents also have a long standing tradition in the initial treatment o NPD. The favorable effect of hydrogen peroxide is mechanical cleaning and the influence on anaerobic bacterial flora of the liberated oxygen

Twice daily rinses with 0.2% chlorhexidine solution to reduce plaque formation, particularly when tooth brushing is not performed

In some cases of NPD the patient response to debridement is minimal or the general health is affected to such an extent that the supplementary use of systemic antibiotics

Supplementary Treatment
Metronidazole 250mg three times daily is the first choice in the treatment of NPD Penicillin 500mg three times daily Tetracycline also effective Topical application of antibiotics is not indicated in the treatment of NPD is not indicated

Non Plaque Induced Inflammatory Gingival Lesions

Gingival inflammation , clinically presenting as gingivitis , is not always due to accumulation of plaque on the tooth surface , and non plaque induced inflammatory gingival reactions often present characteristic clinical features

They may occur due several causes , such as specific bacterial , viral , or fungal infection without an associated plaque related gingival inflammatory reaction

Gingival lesions of genetic origin are seen in hereditary gingival fibromatosis , and several mucocutaneous disorders manifest as gingival inflammation ( Lichen planus , pemphigoid , pemphigus vulgaris and erythema multiforme )

Gingival Diseases Of Specific Bacterial Origin

Infective gingivitis and Stomatitis may occur on rare occasions in both immunocompromised and non immunocompromised individuals
Necrotizing Stomatitis in mandibular left molar area

This lesions are due to infections with: -Neisseria gonorrhea -Treponema pallidum -Streptococci -Mycobacterium chelonae

The gingival lesions manifest

Fiery red edematous painful ulcerations Asymptomatic chancres or mucous patches Highly inflamed gingivitis Biopsy supplemented by microbiologic examination reveals the background of the lesions

Gingival Diseases Of Viral Origin

A number of viral infections are known to cause gingivitis . The most important are herpes viruses. 1) Herpes simplex viruses type 1. 2) Herpes simplex viruses type 2 3) Varicella zoster virus

These viruses usually enter the human body in childhood and may give rise to oral mucosal disease followed by periods of latency and sometimes reactivation

Herpes simplex virus type 1 usually causes oral manifestations

Herpes simplex virus type 2 is mainly involved in anogenital infections and only occasionally is involved in oral infection

Treatment Of Herpetic Gingivostomatitis

Treatment includes careful plaque removal to limit bacterial super infection of the ulcerations , which delay their healing. In severe cases , including patients with immunodeficiency , the systemic use of antiviral drugs such as Acyclovir or Valacyclovir is recommended

Gingival Diseases Of Fungal Origin

Fungal infection of the oral mucosa includes a range of diseases such as aspergillosis , blastomycosis , candidosis , coccidioidomycosis , cryptococcosis , histoplasmosis , mucormycosis and paracoccidioidoycosis infections . Not all of them manifest as gingivitis

Candidosis
Various Candida species are recovered from the mouth of humans including Candida Albicans ; Candida glabrata ;Candida krusei Candida tropicalis ; Candida parapsilosis ; Candida guillermondii . Candida Albicans is the most common

Candida Albicans
The prevalence of oral carriage of Candida Albicans in healthy adults ranges from 3% to 48%. The proportion of Candida Albicans in total yeast population can reach about 50%-80%

Invasion and increased desquamation is due to hyluronidase production. Infection by Candida Albicans usually occurs as a consequence of reduced host defense posture including immunodeficiency , reduced saliva secretion , smoking and treatment with corticosteroids .

Disturbances in the oral microbial flora , such after therapy with broad spectrum antibiotics may also lead to oral candidosis

Healthy individuals oral candidosis rarely manifests in the gingiva. Candida Albicans is frequently isolated from Subgingival flora of patients with severe periodontitis

Various types of oral mucosal manifestations are pseudopseudomembranous candidosis erythematous candidosis , plaque type candidosis , and nodular candidosis

Pseudomembranous candidosis shows whitish patches , which can be wiped off the mucosa with an instrument or gauze leaving a slightly bleeding surface. This type has no major symptoms. Erythematous lesions can be found anywhere in the oral mucosa

The intensely red lesions are usually associated with pain , sometimes with severe pain

The plaque type of oral candidosis is a whitish plaque , which cannot be removed. There are usually no symptoms and the lesion is clinically indistinguishable from oral leukoplakia

Nodular candidal lesions are infrequent in the gingiva. Slightly elevated nodules of white reddish color characterize them

Diagnosis of Candidal Infection

Can be accomplished on the basis of culture smear , and biopsy

Treatment
Topical treatment involves application of antifungal such as nystatin , amphotericin B , or miconazole. Nystatin may be used as an oral suspension Miconazole exits as an oral gel , it should not be given during pregnancy and it can interact with anticoagulants and phenytoin. The treatment in the severe or generalized forms also involves systemic antifungal such as fluconazole

Aphtous recurrent gingivostomatitis Canker Sores

White swellings that change into ulcers surrounded by an area of redness. Appearing suddenly , their most painful last three to six days. Canker sores are more common in women and usually begin to appear by age of twenty. The attacks decrease with age

The cause of canker sores has never been proven , predisposing factors in some people may include deficiencies in iron , folic acid , vitamin B12 , B12 genetic tendency , trauma , cigarette smoking , allergies to certain foods , stress , and immunologic factors

Conventional Treatment
Mouth rinse such as dexamethazone Topical preparations Mild pain relievers Corticosteroids Antibiotics and vaccines have not been proved beneficial Blood analysis will indicate if deficiencies of vit . B12, iron ,folic acid are present

Percoronitis

Percoronitis is a special type of acute periodontal abscess that occurs when gingival tissue (operculum) overlies an erupting tooth (usually a third molar, also known as a wisdom tooth). Recurring acute symptoms are usually initiated by trauma from the opposing tooth or by impaction of food or debris under the flap of tissue that partially covers the erupting tooth

Procedure for relieving the pain is surgical removal of the operculum. inject local anesthetic directly into the overlying tissue and then cut it away using the outline of the tooth as a guide for the incision. Sutures are not required

Irrigate with a weak (2%) hydrogen peroxide (2 solution. Purulent material can be released by placing the catheter tip of the irrigating syringe under the tissue flap overlying the impacted molar.

Prescribe oral analgesics for comfort as well as penicillin over the next 10 days (penicillin VK 500mg ). 500mg Instruct the patient on the importance of cleansing away any food particles that collect beneath the gingival flap. This can be accomplished by simply using a soft toothbrush or by using water jet irrigation

FollowFollow-up should be provided to observe the resolution of the acute infection and to evaluate the need for removal of the gingival flap or molar.

Do not undertake any major blunt dissection while draining pus. This could spread a superficial infection into the deep spaces of the head and neck or follow a deep abscess posteriorly into the carotid sheath