This document provides an overview of necrotizing ulcerative gingivitis (NUG) and necrotizing ulcerative periodontitis (NUP). It discusses the history and epidemiology of these conditions, describing outbreaks among military troops. Clinically, NUG presents as ulcerated and necrotic gingival tissue with characteristic punched out lesions. Untreated, it can progress to involve the underlying bone as NUP. Predisposing factors include poor oral hygiene, preexisting gingivitis, smoking, nutritional deficiencies, systemic illnesses, fatigue, stress and immunodeficiencies. Microorganisms play a role in conjunction with an impaired host response.

1. NECROTIZING ULCERATIVE GINGIVITIS AND NECROTIZING ULCERATIVE PERIODONTITIS
BDS-3rd
year (2019-2020)-Periodontics Lecture
Prof(Dr) Vivek kumar Sharma 15 April 2020
Introduction:
• Necrotizing ulcerative gingivitis (NUG) , necrotizing ulcerative periodontitis(NUP), necrotizing stomatitis (NS) are
the most severe inflammatory periodontal disorders caused by plaque bacteria.
• They are rapidly destructive & debilitating & represents various stages of same disease process (Horning & Cohen
1995). 1986 – Necrotizing ulcerative gingiva-periodontitis 1989 – NUP ( World workshop of Clinical Periodontics )
1999 – Classification of Periodontal Diseases – NUG & NUP , included under the broader classification of Necrotizing
Ulcerative Periodontal Diseases
• Fourth century BC, Xenophon mentioned that Greek soldiers were affected with “sore mouth” and foul-
smelling breath • In 1778, John Hunter described the clinical findings and differentiated ANUG from scurvy
and chronic destructive periodontal disease • ANUG occurred in epidemic form in the French army in the 19th
century
• In 1886, Hersch, a German pathologist, discussed some of the features associated with the disease such as
enlarged lymph nodes, fever, malaise and increased salivation • In 1890s, Plaut and Vincent described the
disease and attributed its origin to fusiform bacilli and spirochetes
NUG often occurs in groups in an epidemic form.
During world war I & II “ epidemics “ broke out among the allied troops. Epidemic like outbreaks
have also occurred among civilian populations. In developing countries, the prevalence of NPD is higher than in
the industrialized countries, & the disease frequently affects the children.
In India, 54- 68 % of NPD cases occurred in children below 10 yrs of age.( Migliani& Sharma 1965;
Pindborg et al 1996). NUG occurs at all ages, with the highest incidence reported between ages 20 & 30 yrs &
ages 15 -20 yrs.
The disease seems to occur slightly more among HIV infected individuals. Studies among groups
of HIV infected individuals have revealed prevalence of NPD between 0 & 27.7%. (Holmstrup & Westergaard1994;
Reichart et al 2003). • NP was found in 1% of 200 HIV seropositive individuals (Riley et al 1992) & the prevalence
may not in fact, differ from much of the general population ( Drinkard et al 1991 );This is particularly true after
introduction of antiretroviral therapy.
Clinical features –
Oral signs • NG – an inflammatory destructive gingival condition,
*Characterized by ulcerated and necrotic papilla and gingival margins. Punched out crater like depressions at the
crest of the interdental papillae is a characteristic feature.
• The surface of the craters is covered by a gray pseudomembranous slough. The sloughed material has little
coherence and is composed of fibrin, necrotic tissue, RBC,WBC, Bacteria.
• Linear erythema demarcating marginal necrosis and the relatively unaffected zone
• In some cases the lesions are denuded of the surface pseudomembrane, exposing the gingival margin which is
red, shiny, & hemorrhagic. The characteristic lesion may progressively destroy the gingiva & underlying periodontal
tissues.
INITIAL PUNCH OUT LESION

2. Spontaneous gingival hemorrhage or pronounced bleeding after the slight stimulation are characteristic clinical
signs.A characteristic & pronounced foetor ex ore is often associated with this disease . Although it is not always
very noticeable. Increased salivation. The palatal/lingual gingiva Is less frequently involved than the facial gingiva
Frequently gingiva of partially impacted tooth are also affected.
In NUP:
Progression of the interproximal lesion often results in destruction of the interdental alveolar bone. Sequestrum
formation: necrosis of a small or large part of the alveolar bone, which is denoted as sequestrum. The bone
fragment is initially immovable, later on it becomes loose. Sequestrum involves interproximal as well as facial or
palatal cortical bone. Involvement of the alveolar mucosa : NS In severe malnutrition or immunocompromised
individual as in HIV, the necrotic process progresses beyond the mucogingival junction affecting the alveolar
mucosa. It may result in extensive denudation of the bone – leading to major sequestration – with the
development of oroantral fistula and osteitis.
Oral Symptoms • The lesion is extremely sensitive to touch, & the patient may often complains of a constant
radiating, gnawing pain that is often intensified by eating spicy or hot foods & chewing. • There is metallic foul
taste & an excessive amount of pasty saliva.
Extra oral & systemic signs & symptoms * In mild & moderate stages of disease Local lymphadenopathy &
slight elevation in temperature. * In severe cases High fever, increased pulse rate, leucocytois, loss of appetite &
general lassitude. *Systemic reactions are more severe in children. *Insomnia, constipation, gastro-intestinal
disorders, headache, & mental depression sometimes accompany the condition.
Stages of oral necrotizing disease – by Horning & Cohen
• Stage 1- necrosis of the tip of the interdental papilla.
• Stage 2- necrosis of entire papilla
• Stage 3- necrosis extending to the gingival margin.
• Stage 4- necrosis extending to the attached gingiva.
• Stage 5– necrosis extending to labial & buccal mucosa.
• Stage 6- necrosis exposing alveolar bone.
• Stage 7– necrosis perforating skin of cheek
ETIOLOGY: It includes
• Role of microorganism
• Role of host response
• Predisposing factors includes
1. Local predisposing factor 2. Systemic predisposing factor
LOCAL PREDISPOSING FACTORS • It includes poor oral hygiene, preexisting gingivitis , injury to gingiva, & smoking • It may also
occur in disease free mouth, it most often occurs superimposed on preexisting chronic gingival disease & periodontal pockets. • Areas of
gingiva traumatized by opposing teeth in malocclusion – may predispose to NUG. • Pindborg et al – 98% of his patients with NUG were
smokers & that the frequency of disease increases with an increase exposure to smoke.
SYSTEMIC PREDISPOSING FACTORS • It includes – nutritional deficiency (malnutrition), – debilitating diseases, – fatigue
caused by chronic sleep deficiency, – psychological stress, – immunodeficiency, – other health habits like alcohol & drug abuse.