Necrotizing Ulcerative Gingivitis PDF

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Summary

Acute lesions in the periodontium, such as abscesses and necrotizing diseases, are among the few clinical situations in periodontics where patients may seek urgent care, mostly because of the associated pain. In addition, and in contrast to most other periodontal conditions, rapid destruction of per...

Description

NECROTIZING ULCERATIVE GINGIVITIS – KEY NOTES Usually identified as an acute disease – MISNOMER NUG often undergoes a diminution in severity without treatment, thereby leading to a subacute stage with milder clinical symptoms. Thus, patients may have a history of repeated remissions and exacerbations, and the condition can also recur in previously treated patients. Involvement may be limited to a single tooth or group of teeth, or it may be widespread throughout the mouth. NUG can cause tissue destruction that involves the periodontal

attachment apparatus,

especially in patients with long-standing disease or severe immunosuppression. When bone loss occurs, the condition is called necrotizing ulcerative periodontitis (NUP)

HISTORY Necrotizing ulcerative gingivitis had been recognized during the fourth century BC by Xenophon, who mentioned that Greek soldiers were affected with “sore mouth and foulsmelling breath.” In 1778, Hunter described the clinical features of this disease and differentiated it from scurvy and chronic periodontitis Necrotizing ulcerative gingivitis was commonly found among the French soldiers in the nineteenth century. Hirsch added secondary findings to the clinical presentation of NUG in 1886 and Bergeron described both acute and chronic forms of the disease in 1895 Hyacinthe Jean Vincent (1862-1950), a French physician working at the Pasteur Institute in Paris, and Hugo Carl Plaut (1858-1928) in Germany described the spirillum and fusiform bacilli associated with what later became known as Vincent’s angina In 1904, Vincent described the presence of these organisms in ulceronecrotic gingivitis

OTHER NAMES 

Vincent’s disease



Vincent’s stomatitis



Vincent’s angina



Plaut – Vincent stomatitis



Fusospirochetal gingivitis



Fusospirillary gingivitis



Trench mouth



Acute ulceromembranous gingivitis



Stomatitis ulcerosa



Fetid stomatitis



Putrid stomatitis



Acute ulcerative gingivitis



Necrotizing gingivitis



Acute necrotizing ulcerative gingivitis or ANUG

ORAL SIGNS Punched-out, craterlike depressions at the crest of the interdental papillae that subsequently extend to the marginal gingiva and rarely to the attached gingiva and oral mucosa covered by a gray, pseudomembranous slough that is demarcated from the remainder of the gingival mucosa by a pronounced linear erythema. In some cases, the lesions are denuded of the surface pseudomembrane, thereby exposing the gingival margin, which is red, shiny, and hemorrhagic. The characteristic lesions may progressively destroy the gingiva and the underlying periodontal tissues 

A fetid odour



Increased salivation



Can occur in otherwise disease-free mouths, or it can be superimposed on chronic gingivitis or periodontal pockets.

ORAL SYMPTOMS The lesions are extremely sensitive to touch Often complains of a constant radiating, gnawing pain that is intensified by eating spicy or hot foods and chewing “metallic” foul taste “pasty” saliva

EXTRAORAL AND SYSTEMIC SIGNS AND SYMPTOMS MILD FORMS – 

Local lymphadenopathy



Slight elevation in temperature



Systemic

reactions

are

more

severe

in

children. Insomnia,

constipation,

gastrointestinal disorders, headache, and mental depression sometimes accompany the condition.



In very rare cases, severe sequelae such as gangrenous stomatitis and noma have been described

CLINICAL COURSE Can vary Staging of NG infections was proposed by Pindborg, who described four stages: 1) only the tip of the interdental papilla was affected 2) marginal gingiva was affected, with punched-out papilla; 3) Attached gingiva was also affected 4) Exposure of bone with complete loss of interdental papilla, marginal gingiva and attached gingiva Uohara similarly suggested three stages of disease: STAGE 1 Acute necrotizing ulcerative gingivitis ; associated with minimal contiguous soft-tissue spread of fusospirochetal infections. STAGE 2 Acute necrotizing ulcerative mucositis or Vincent’s angina STAGE 3 Gangrenous stomatitis and agranulocytic ulcerations; deep necrotizing fusospirochetal infections Horning and Cohen STAGE1: Necrosis of the tip of the interdental papilla (93%) STAGE 2: Necrosis of the entire papilla (19%) STAGE 3: Necrosis extending to the gingival margin (21%) STAGE 4: Necrosis extending also to the attached gingiva (1%) STAGE 5: Necrosis extending into buccal or labial mucosa (6%) STAGE 6: Necrosis exposing alveolar bone (1%) STAGE 7: Necrosis perforating skin of cheek (0%)

HISTOPATHOLOGY Microscopically, the NUG lesion is a nonspecific acute necrotizing inflammation of the gingival margin that involves both the stratified squamous epithelium and the underlying connective tissue

The surface epithelium is destroyed and replaced by a meshwork of fibrin, necrotic epithelial cells, polymorphonuclear leukocytes (neutrophils) (PMNs), and various types of microorganisms At the immediate border of the necrotic pseudomembrane, the epithelium is edematous, and the individual cells exhibit varying degrees of hydropic degeneration In addition, there is an infiltration of PMNs in the intercellular spaces. The underlying connective tissue is markedly hyperemic, with numerous engorged capillaries and a dense infiltration of PMNs. This acutely inflamed zone appears clinically as the linear erythema beneath the surface pseudomembrane. Numerous plasma cells may appear in the periphery of the infiltrate; this is interpreted as an area of established chronic gingivitis on which the acute lesion became superimposed. The epithelium and connective tissue alterations decrease as the distance from the necrotic gingival margin increases, blending gradually with the uninvolved gingiva. Hooper et al in 1979 conducted a preliminary histological and immunofluorescent investigation of the edge of the ulcer in acute ulcerative gingivitis. The results of this study show that the lesion is dominated by polymorphonuclear leukocytes, with plasma cells present in the deeper parts. The epithelium on the edge shows widening of the intercellular spaces with destruction of the epithelial cells, accompanied by a heavy infiltrate of PMNs. Both IgG and C3 could be demonstrated between these epithelial cells. The histopathogenesis of AUG therefore seems to involve a PMN infiltration of the epithelium, with subsequent destruction of the epithelium, probably due to the release of hydrolytic enzymes. The presence of the PMNs within the epithelium may involve direct bacterial Chemotaxis and/or the activation of complement via the classical or alternative pathways.

RELATION OF BACTERIA TO THE NECROTIZING ULCERATIVE GINGIVITIS LESION The bacterial etiology was first proposed by Plaut in 1894 and Vincent in 1896 Working independently, they both reported that fusiform-spirochete bacterial flora were associated with the lesions of necrotizing ulcerative gingivitis. Even though fusiforms and spirochetes are commonly found in patients who do not have NUG it does appear that these and perhaps other bacteria play a major role in the pathogenesis of NUG. First, electron microscopic studies of gingival biopsies from NUG patients have provided some of the most

well known findings in support of bacterial invasion in a periodontal disease. In a classic with the gingival lesion of NUG were identified electron microscopic investigation in 1965, four zones associated BACTERIAL ZONE: composed of a large mass of bacteria with varying morphotypes, including some spirochetes. NEUTROPHIL RICH ZONE: underlies the bacterial zone, contains many leukocytes with neutrophils predominating. Bacteria, including many spirochetes, are located between the cells. NECROTIC ZONE: characterized by disintegrating cells and many spirochetes (large and intermediate) and other bacteria that appear to be fusiforms SPIROCHETAL INFILTRATION ZONE: tissue elements appear well preserved but are infiltrated by spirochetes, both large and intermediate in size. No other bacteria were observed. Spirochetes have been found as deep as 300 μm from the surface. The majority of spirochetes in the deeper zones are morphologically different from cultivated strains of Treponema microdentium. They occur in non-necrotic tissue before other types of bacteria, and they may be present in high concentrations intercellularly in the epithelium adjacent to the ulcerated lesion and in the connective tissue In a study conducted on biopsies from eight patients with pathognomonic signs of ANUG by Courtois et al in 1983, it was found that (1) both spirochetes and other morphologically different bacteria are capable ofinfiltrating viable connective tissue; (2) the bacterial penetration can occur up to a depth of 400 µ , as measured from the apical cell membrane ofthe nearest basal epithelial cell; Microbial studies have also characterized the genera and species of the cultivable flora in NUG The constant cultivable flora consisted of a limited number of predominant organisms, B. melaninogenicus ssp. intermedius, now known as Prevotella intermedia, and Fusobacterium sp. Microscopically, Treponema and Selenomonas sp. comprised the constant flora The concept of a predominant constant flora suggests an association of these flora with the disease. As with other periodontal diseases however, this association does not necessarily demonstrate an etiologic role for these bacteria in the initiation of NUG.

DIAGNOSIS Diagnosis is based on clinical findings of gingival pain, ulceration, and bleeding. A bacterial smear is not necessary or definitive, because the bacterial picture is not appreciably different from that of patients with marginal gingivitis, periodontal pockets, pericoronitis, or primary herpetic gingivostomatitis The microscopic examination of a biopsy specimen is not sufficiently specific to be diagnostic. It can be used to differentiate NUG from specific infections (e.g., tuberculosis) or from neoplastic disease, but it does not differentiate between NUG and other necrotizing conditions of nonspecific origin, such as those produced by trauma or caustic medications.

DIFFERENTIAL DIAGNOSIS 

Primary herpetic gingivostomatitis



Desquamative gingivitis



Chronic destructive periodontal disease



Diphtheria



Syphilis



Traumatic conditions

ETIOLOGY 

Plaut in 1894 and Vincent in 1896 postulated that NUG was caused by specific bacteria: fusiform bacillus and a spirochetal organism.



Spirochetal organisms and fusiform bacilli are always found in patients with the disease, with other organisms also involved



Rosebury and colleagues described a fusospirochetal complex that consists of T. microdentium, intermediate spirochetes, vibrios, fusiform bacilli, and filamentous organisms in addition to several Borrelia species.



Loesche and colleagues in 1982 described a predominant constant flora and a variable flora associated with NUG. The constant flora is composed of Prevotella intermedia in addition to Fusobacterium, Treponema, and Selenomonas species. The variable flora consists of a heterogeneous array of bacterial types.



Treatment with metronidazole results in a significant reduction of Treponema species, Prevotella intermedia, and Fusobacterium, with resolution of the clinical symptoms.



The antibacterial spectrum of this drug provides evidence for the anaerobic members of the flora as etiologic agents.



Plaque samples from 22 ulcerated sites in eight patients with ANUG were cultured using quantitative anaerobic procedures and were examined microscopically. The partial characterization of the predominant cultivable flora revealed a constant flora comprised of a limited number of bacterial types and a variable flora composed of a heterogeneous array of bacterial types.



This constant flora would appear to be pathognomonic of acute necrotizing ulcerative gingivitis (ANUG) and included the various Treponema and Selenomonas sp., which comprised about 32 and 6%, respectively, of the microscopic count; B. melaninogenicus ssp. Intermedius and Fusobacterium sp., which averaged 24 and 3%, respectively, of the viable count.



One week of metronidazole treatment caused a prompt resolution of clinical symptoms, which coincided with a significant reduction in the plaque proportions of the Treponema sp., B. melaninogenicus ssp., intermedius and Fusobacterium sp. for at least 2 to 3 months following treatment.



Thus, the same anaerobic species which were numerically associated with the ANUG lesion were also selectively reduced in the plaque flora following resolution of the infection.



Thus it was proposed that these particular anaerobic species gained ascendency in the plaque as a result of being selected through the availability of host-derived nutrients in individuals who had undergone certain physiological and psychological stresses.



These bacteriologic findings have been supported by immunologic data that demonstrated increased immunoglobulin G and M antibody titers for medium-sized spirochetes and P. intermedia in patients with NUG as compared with titers in those patients with chronic gingivitis and healthy controls



Chung et al in 1983 conducted a study to elucidate the humoral immune response in ANUG, the serum IgG and IgM antibody levels to the predominant infecting bacteria of the initial and convalescent stages of ANUG .



Compared to the gingivitis and healthy groups, the ANUG groups exhibited significantly higher IgG and IgM titers to intermediate-sized spirochetes and higher IgG titers to Bacteroides melaninogenicus subsp intermedius.



Thus it was concluded that these organisms are major bacterial components in ANUG lesions. They also suggested that these bacteria proliferate above-normal levels several weeks or months prior to the clinical onset of ANUG.

ROLE OF THE HOST RESPONSE 

The role of an impaired host response in NUG has long been recognized.



NUG has not been produced experimentally in humans or animals by only the inoculation of bacterial exudates from the lesions.



NUG is not found in well-nourished individuals with a fully functional immune system.All

of

the

predisposing

factors

for

NUG

are

associated

with

immunosuppression. 

Depression in host defense mechanisms, particularly in PMN chemotaxis and phagocytosis, in patients with NUG have been described.



Increased

cortisol

levels

have

been

associated

with

a

depression

of

polymorphonuclear leukocyte (PMN) function 

Depressed PMN function as measured by chemotactic, phagocytic, and bactericidal abilities has been reported in NUG patients



In addition, altered lymphocyte function has been reported in NUG



It has also been suggested that elevated steroid levels may provide essential nutrients for specific bacterial growth (Prevotella intermedia)



Cogen et al in 1982 conducted a study on patients with ANUG to assess the polymorphonuclear leukocyte responsiveness to chemotaxis and phagocytosis and lymphocyte responsiveness to stimulation by nonspecific mitogens.



The results from the study revealed that ANUG patients displayed significantly depressed

responsiveness in both Chemotaxis and phagocytosis, compared to the

controls. 

There was also reduced DNA synthesis by ANUG patients' lymphocytes upon stimulation by a nonspecific mitogen (Con A). The data presented in this report suggest that depression of some host defense mechanisms, particularly Chemotaxis and phagocytosis, may be important in the pathogenesis of ANUG.



Immunodeficiency may be related to varying levels of nutritional deficiency, fatigue caused by chronic sleep deprivation, other health habits (e.g., alcohol or drug abuse), psychosocial factors, or systemic disease. Importantly, NUG may be the presenting symptom for patients with immunosuppression related to human immunodeficiency virus infection.



A multitude of oral lesions have been described in individuals infected with the human immunodeficiency virus (HIV). Few studies have attempted to correlate

specific oral findings with immune status and HIV disease progression in the population reflecting the demographic profile of this epidemic. 

Glick et al in 1994 conducted a prospective among 700 ambulatory HIV-infected individuals seeking dental care.



The association between NUP diagnosis and CD4+ cell count below 200 cells/mm3 was also investigated, and it was found that HIV-infected individuals presenting with a diagnosis of NUP were 20.8 times as likely to have a CD4+ cell count below 200 cells/mm3 compared to HIV-infected individuals presenting without NUP. The prevalence of NUP was 6.3%.



The presence of NUP in HIV-infected individuals was considered a predictable marker for immune deterioration and disease progression. Specific oral lesions such as NUP should be considered for inclusion within the AIDS surveillance definition.



Some reports have described an increased incidence of NUG among HIV-infected individuals, although this has not been substantiated by other studies.



There is no consensus regarding whether the incidence of NUG increases in HIVpositive patients. However, a recent study evaluated the HIV status of individuals who presented with necrotizing periodontal diseases, and 69% were found to be HIV seropositive.



The treatment of NUG in these patients does not differ from that used for HIVnegative individuals



Shangase et al in 2004 conducted a study to determine a possible correlation between NUG/NUP and HIV infection in the as yet undiagnosed patients.



86 systemically asymptomatic patients were diagnosed with NUG/NUP. All patients were treated with 400 mg of metronidazole and 500 mg paracetamol, three times a day for five days. Mechanical debridement under local anesthesia was performed five days after the initial consultation. The possible involvement of HIV-infection was explained and patients were advised to have a blood test taken.



Results from the study revealed that NUG/NUP in otherwise systemically healthy individuals is strongly correlated with HIV infection, with a predictive value of 69.6 per cent

and therefore it is recommended that patients presenting with these

conditions be encouraged to undergo testing to establish their HIV status for appropriate referrals and management.



Acute necrotising ulcerative gingivitis (ANUG), usually seen in malnourished children and in advanced HIV infection, can b...