Necrotizing Ulcerative Gingivitis Necrotizing ulcerative periodontitis

Definition

A microbial disease of the gingiva in the context of an impaired host response. It is characterized by the death

and sloughing of gingival tissue and presents with characteristic signs and symptoms.

May be an extension of NUGinto the periodontal structures, leading to periodontal attachment and

bone loss.

Clinical Features

NUG often undergoes a diminution in severity without treatment, leading to a subacute stage with milder clinical symptoms. Thus patients may have :

o a history of repeated remissions and exacerbations

o Edematous interdental papillaeo Crateriform lesions, most commonly in the

anterior incisor and posterior molar regionso Erythemao Spontaneous gingival hemorrhageo Necrosis with formation of a grayish

pseudomembrane over affected areao Pain with rapid onseto Halitosiso Blunted gingivae between the teeth

(normally cone-shaped)o Often accompanied by fever, malaise, and

lymphadenopathyo Often associated with immunosuppression,

tobacco use, and physical or emotional stress; the vernacular name 'trench mouth' came from large outbreaks in the World War I trenches. The disease is also seen in

o clinical cases of NUP are defined by necrosis and ulceration of the coronal portion of the interdental papillae and gingival margin, with a painful, bright red marginal gingiva that bleeds easily . Show gingival crater on interdental papillae. NUP characterized by destructive progression

o NUP distinguished by : the destructive progression of the

disease that includes periodontal attachment and bone loss.

Deep interdental osseous craters demonstrate periodontal lesions of NUP.

Gingival lesion destroys the marginal epithelium and connective tissue, resulting in gingival recession.

Periodontal pockets are formed because the junctional epithelial cells remain viable and can therefore migrate apically to cover areas of connective tissue loss.

Tooth mobility Ultimately tooth loss. NUP patient may present with : Oral

college dormitories and other stressful crowded living conditions, but there is no evidence that acute necrotizing ulcerative gingivitis is communicabl

malodor ( foul odor ) Fever Malaise lymphadenopathy

Microscopic Findings

Surface epithelium is destroyed and replaced by a meshwork of fibrin, necrotic epithelial cells,

polymorphonuclear leukocytes (PMNs, neutrophils), and various types of microorganisms individual cells exhibit varying degrees of hydropic

degeneration.

Commonly similar to NUG 1 - surface biofilm composed of a mixed microbial flora with

different morphotypes and a subsurface flora with dense aggregations of spirochetes

( bacterial zone ). 2 - Dense aggregations of PMNs ( neutrophil-

rich zone ) . 3 - N ecrotic cells ( necrotic zone ). 4 - S pirochetal infiltration zone.

5 - High levels of yeasts and herpes-like viruses were observed

Etiology Build-up of bacterial plaque on the teeth,

adjacent gingivae, and pockets between teeth

and gums, releasing toxins that cause an

inflammatory response (most common

species involved are Gram-negative anaerobic

bacteria—Actinobacillus

actinomycetemcomitans and Porphyromonas

gingivalis)

Build-up of calculus contributes to the chronicity

Etiology of NUP Generally as NUG: 1- Bacteria role: NUP in HIV-positive

patients demonstrated significantly greater numbers of the opportunistic fungus Candida albicans and a higher prevalence of A. actinomycetemcomitans , P. intermedia , P. gingivalis , Fusobacterium nucleatum , and Campylobacter species compared with HIV-negative controls . L ow or variable level of spirochetes , which is inconsistent with the flora associated with NUG .

2- Immunocompromised Status : Clearly,

of periodontal disease; if plaque is not removed, it

forms a hard mass commonly called 'tartar,' which

traps bacteria that cause gingivitis. Toxins

released from the bacteria stimulate an immune

response (via cytokines) that increases production

of collagenase. Untreated, this has a destructive

effect on the connective tissue, which renders the

teeth less secure, leading to periodontal disease

and tooth loss

Smoking tobacco

Faulty dental prosthesis

Malocclusion

Breathing through the mouth

Local trauma (eg, an overly aggressive

toothbrushing technique)

Dry mouth: because of loss of protective effect of

saliva

Vitamin deficiency, especially of vitamin C

both NUG and NUP lesions are more prevalent in patients with compromised or suppressed immune systems. Commonly in HIV-positive and AIDS patients.

3- Psychologic Stress Stress increases systemic cortisol levels , and sustained increases in cortisone have a suppressive effect on the immune response by microcirculation in gingiva and altered phagocytic functions. Some researchers: F ound that urinary levels of 17-hydroxycorticosteroid were higher in subjects with NUG than in all other subjects diagnosed with periodontal health , gingivitis , or periodontitis

4- Malnutrition Direct evidence of the relationship between malnutrition and necrotizing periodontal disease is limited to descriptions of necrotizing infections in severely malnourished children. M any of the host defenses , including phagocytosis; cell-mediated immunity ; and complement, antibody , and altered cytokine production , are impaired in malnourished individuals

5- Reduction of nutrients to cells and tissues results in immunosuppression and disease susceptibility. Malnutrition can predispose an individual to opportunistic infections or intensify the

severity of current oral infections6- Other factors - Smoking - Plaque and

other local factors e.g. calculus

Predisposing factors

Preexisting gingivitis, injury to the gingiva, smoking , nutritional deficiency; fatigue caused by chronic sleep deficiency; other health habits

(e.g., alcohol or drug abuse), and systemic disease (e.g., diabetes, debilitating infection).

Poor oral hygiene, preexisting periodontal disease, smoking, viral infections,

immunocompromised status, psychosocial stress, and malnutrition

Complication

Andcomorbiditi

es

If oral hygiene is poor, plaque accumulates and can form calculus; both harbor toxin-releasing bacteria around the gum line. Eating carbohydrate-containing foods promotes an acid environment in the mouth that encourages bacterial growth

Crowns or fillings that are poorly contoured provide traps for food particles

Smoking has a significant effect on overall dental health

Coexisting diseases such as diabetes mellitus Down syndrome, and HIV infection render a patient more susceptible to the inflammatory process

Degenerative disease of the connective tissue such as rheumatoid arthritis, systemic lupus erythematosus, and CREST syndrome (calcinosis, Raynaud phenomenon, esophageal dysfunction, sclerodactyly, and telangiectasia) may make a person more susceptible to periodontal disease

Sjögren syndrome or xerostomia can cause dryness of the mouth, which increases the likelihood of oral pathology

Steroid medication may increase a patient's

Gangrenous (necrotic) stomatitis :

extensive necrotic process to

adjacent gingival mucosa (check,

palate, tongue, floor of m., lips)

Noma ( cancrum oris ): serious (fatal )

form of necrotic stomatitis that lead

to exposure of bone and perforation

of check & nasal cavity

susceptibility to bacteria Ill-fitting dentures or restorations should be properly

fitted

Treatment

Treatment usually is divided into the acute phase and the

maintenance phase. The primary concern in the acute phase is

pain control. For the maintenance phase, treatment is directed

toward reducing the burden of potential pathogens, preventing

further tissue destruction, and promoting healing.

For uncomplicated NUP or NUG, the primary care provider should prescribe an antimicrobial rinse , antibiotic therapy , medications for pain management, and nutritional supplementation; the patient should be referred to a dental health care professional.

Chlorhexidine gluconate rinse (0.12%) twice daily after brushing and flossing (an alcohol-free preparation is preferred).

Antibiotic therapy (preferably narrow spectrum, to leave gram-positive aerobic flora unperturbed).

Refer to a dentist for the following:

Removal of plaque and debris from the site of infection and inflammation.

Debridement of necrotic hard and soft tissues, with a 0.12% chlorhexidine gluconate or povidone-iodine lavage

The treatment is mostly similar to NUG 1- Lavage of necrotic tissue and

pseudomembrane under local anesthesia. 2 - Correction of the systemic condition as possible and consultation with patient’s physician . 3- Periodontal debridement ( scaling and root planing ).4- Local and systemic antibiotics 5- Antiseptic mouth wash ( chlorhexidine ) 6 - Antifungal and antiviral drugs

7- Good nutrition and enhancement the psychic status.

8 - Oral hygiene instruction and patient motivation to control dental plaque.

9 - Maintenance recall visits to evaluate periodontal health and observe the recurrence of lesions.