Necrotizing ulcerative gingivitis (NUG) and necrotizing ulcerative periodontitis (NUP) are microbial diseases characterized by the death of gingival tissue and can lead to significant periodontal destruction and tooth loss, particularly in immunocompromised individuals. Clinical features include painful ulcerations, malodor, and systemic symptoms such as fever and lymphadenopathy, while contributing factors include poor oral hygiene, smoking, malnutrition, and psychological stress. Treatment focuses on pain management, antimicrobial therapy, and addressing underlying conditions to prevent further tissue damage and promote healing.

1. 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 papillae
o Crateriform lesions, most commonly in the
anterior incisor and posterior molar regions
o Erythema
o Spontaneous gingival hemorrhage
o Necrosis with formation of a grayish
pseudomembrane over affected area
o Pain with rapid onset
o Halitosis
o Blunted gingivae between the teeth (normally
cone-shaped)
o Often accompanied by fever, malaise, and
lymphadenopathy
o Often associated with immunosuppression,
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.

2. 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 college dormitories
and other stressful crowded living conditions,
but there is no evidence that acute necrotizing
ulcerative gingivitis is communicabl
 Tooth mobility Ultimately tooth loss.
 NUP patient may present with : Oral
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
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

3. actinomycetemcomitans and Porphyromonas gingivalis)
 Build-up of calculus contributes to the chronicity 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
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, 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-

4. saliva
 Vitamin deficiency, especially of vitamin C
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
infections
6- 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
And
comorbidities
 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
 Gangrenous (necrotic) stomatitis :
extensive necrotic process to adjacent
gingival mucosa (check, palate, tongue,
floor of m., lips)

5.  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 susceptibility
to bacteria
 Ill-fitting dentures or restorations should be properly
fitted
 Noma ( cancrum oris ): serious (fatal )
form of necrotic stomatitis that lead to
exposure of bone and perforation of
check & nasal cavity
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.
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.  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
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.