Necrotizing Ulcerative Stomatitis

Other names
Types
Causes
Symptoms
Diagnostic tests
Non-pharmacological treatments (therapies & other care)
Drug treatments
Dietary molecular supplements
Immunity-support / regenerative” drug domains
Surgeries (what they are and why done)
Preventions
When to see a doctor urgently
What to eat and what to avoid (during healing)
FAQs

Necrotizing ulcerative stomatitis is a severe mouth infection. The soft lining of the mouth dies in patches, and deep ulcers form. These ulcers can cut across the gums, cheeks, and other mouth tissues. The infection is fast and painful. It often starts as necrotizing gingivitis (painful, bleeding gums), then spreads into the deeper tissues. In the worst cases, it can progress to noma (cancrum oris), which destroys parts of the face. Doctors group NUS with the necrotizing periodontal diseases—a spectrum that includes necrotizing gingivitis, necrotizing periodontitis, and necrotizing stomatitis. NCBI+1

Necrotizing ulcerative stomatitis is a fast-moving infection that destroys the gums, the soft lining of the mouth, and sometimes the jawbone. It belongs to the same disease family as necrotizing gingivitis and necrotizing periodontitis; clinicians think of these as steps on one spectrum. When the infection becomes very aggressive in vulnerable people (for example, in children with severe malnutrition or people with immune weakness), it can extend through the cheeks and lips and become noma (cancrum oris), a life-threatening gangrene of the face. Common signs include sudden mouth pain, gray-white dead tissue, foul breath, easy bleeding, fever, and swollen nodes below the jaw. Early treatment and nutrition stop the disease in most cases. NCBI+1

NUS happens when mouth bacteria overwhelm the body’s defenses. It is not due to a single germ. It is usually polymicrobial, with anaerobic bacteria such as fusobacteria and spirochetes involved, acting together when the immune system is weak. Poor oral hygiene, malnutrition, infections, and other stresses on the body raise the risk. NCBI+1

NUS can occur at any age but is most feared in settings of extreme poverty, crowding, and poor nutrition. In those settings, the same disease spectrum can lead to noma, now officially recognized by WHO as a neglected tropical disease because of its severity and link to poverty, malnutrition, and immune weakness. World Health Organization+1

Other names

Doctors and textbooks have used several overlapping names. You may see:

Necrotizing stomatitis (preferred modern dental term when necrosis extends beyond the gums into oral mucosa). aap.onlinelibrary.wiley.com
Necrotizing ulcerative stomatitis (NUS) (older wording that emphasizes the ulcers). NCBI
Vincent’s stomatitis or “fusospirochetal” disease (historical terms linked to the bacteria first described). Wikipedia
Noma / cancrum oris (the destructive end-stage of the same process in extreme settings). World Health Organization

Types

Clinicians think of three stages in one pathologic process, based on how far the necrosis extends:

Necrotizing gingivitis (NG) – very painful, bleeding gums, “punched-out” papillae between teeth. NCBI
Necrotizing periodontitis (NP) – same infection with loss of attachment and bone involvement around teeth. NCBI
Necrotizing stomatitis (NS / NUS) – necrosis spreads past the gums into the oral mucosa, sometimes to bone; may progress to noma if not controlled. aap.onlinelibrary.wiley.com+1

This staged view is endorsed by modern periodontal classifications (2017 World Workshop). aap.onlinelibrary.wiley.com

Causes

Polymicrobial oral infection
Many different mouth bacteria, especially anaerobes like fusobacteria and spirochetes, act together. No single germ is enough by itself. The mix thrives when tissues are weak and oxygen is low. NCBI+1
Poor oral hygiene
Plaque and food debris feed harmful bacteria. When not cleaned, toxins irritate gums and mucosa, making tissue easier to destroy. NCBI
Malnutrition (protein-energy and micronutrient lack)
Lack of calories, protein, and vitamins weakens immunity and slows healing, allowing infection to spread and tissue to die. World Health Organization
Underlying infections (e.g., measles, malaria, respiratory infections)
Intercurrent infections drain the immune system and tip the balance toward tissue necrosis in the mouth. World Health Organization
Immunosuppression (e.g., HIV infection)
Low white-blood-cell defenses and altered oral flora increase risk and severity of necrotizing periodontal diseases. NCBI
Extreme poverty and crowding
Limited access to food, clean water, and dental care create the conditions in which the disease thrives. World Health Organization
Psychological stress and sleep deprivation
Stress hormones can impair local immunity and salivary flow, letting pathogenic bacteria overgrow. Wikipedia
Tobacco use
Smoking reduces blood flow to gums, alters host response, and favors anaerobes that drive necrosis. Wikipedia
Alcohol misuse
Alcohol can dry the mouth, impair nutrition, and weaken systemic immunity, increasing susceptibility. Wikipedia
Pre-existing gingivitis or periodontitis
Inflamed gums are already damaged and easier for necrotizing infection to penetrate. NCBI
Local trauma (cheek biting, sharp teeth, rough dental appliances)
Small wounds in the mucosa create entry points for bacteria and necrosis. NCBI
Poor sanitation and unsafe water
Reinforces malnutrition and infection cycles that weaken the host and oral tissues. World Health Organization
Low saliva flow (dehydration, febrile illness, medications)
Dry mouth loses natural antibacterial action and buffering, allowing rapid bacterial growth. MSD Manuals
Recent viral illness
After viral infections, the immune system is temporarily down, so bacteria in the mouth can overrun tissues. World Health Organization
Young age in high-risk settings
Children in the 2–6 year range in impoverished areas are especially vulnerable to the severe end of the spectrum (noma). World Health Organization
Systemic inflammatory burden
High background inflammation (e.g., untreated infections) can prime tissues for necrosis under bacterial attack. World Health Organization
Vitamin deficiencies (A, C, B-complex)
These vitamins support epithelial integrity and immune function; deficiency weakens barriers and repair. World Health Organization
Untreated dental pain leading to poor oral intake
Pain makes eating and brushing difficult, worsening nutrition and hygiene and accelerating the cycle. MSD Manuals
Limited access to timely dental/medical care
Delayed debridement and antibiotics allow spread from gums into oral mucosa and bone. MSD Manuals
Co-existing systemic disease (e.g., hematologic disorders)
Illnesses that reduce neutrophil function or blood supply make necrosis more likely and more severe. NCBI

Symptoms

Severe mouth pain
The pain is sudden and sharp. It worsens with chewing and brushing. It is much stronger than typical gingivitis pain. NCBI
Bleeding gums and mucosa
Even light touch can cause bleeding because the surface tissue is inflamed and fragile. MSD Manuals
“Punched-out” or crater-like sores
Ulcers have a gray surface and a red rim. In NUS, they extend beyond the gum to the cheek or other lining tissues. NCBI+1
Dead tissue (necrosis) with gray pseudomembrane
A foul-smelling layer covers the ulcers. Under it, tissue is dying. NCBI
Bad breath (halitosis)
Rotting tissue and anaerobic bacteria create a strong odor. Wikipedia
Swollen, tender gums and oral mucosa
Inflammation and bacterial toxins make tissues puffy and painful to touch. MSD Manuals
Fever and malaise
The body reacts to infection with fever, fatigue, and loss of energy. Wikipedia
Lymph node swelling under the jaw or in the neck
Nodes enlarge as they filter bacteria and debris from the infected area. Wikipedia
Difficulty chewing and swallowing
Pain and swelling limit jaw movement and make eating hard. MSD Manuals
Trismus (reduced mouth opening)
Muscle spasm and pain can limit opening, especially when the infection spreads. NCBI
Loose teeth if bone is involved
If necrosis reaches periodontal ligament and bone, teeth may feel mobile. NCBI
Ulcer edges that spread quickly
Without care, ulcers can enlarge in days and cross tissue planes. NCBI
Loss of appetite and weight loss
Pain and fever reduce intake, which further worsens nutrition. World Health Organization
Dehydration signs (dry mouth, dizziness)
Ill children and adults may drink less; dehydration worsens dry mouth and infection. MSD Manuals
In severe cases, progression toward facial tissue loss (noma)
If untreated in high-risk settings, NUS can progress beyond the mouth and destroy parts of the face. NCBI+1

Diagnostic tests

A) Physical examination (bedside / in the chair)

Full oral inspection under light
The clinician looks for punched-out ulcers, gray slough, red rims, and tissue death extending beyond the gums. The pattern helps separate NUS from simple gingivitis or herpetic sores. NCBI+1
Smell assessment (organoleptic halitosis check)
A strong fetid odor is common with anaerobic necrosis and supports the diagnosis in the right setting. Wikipedia
Fever and vital signs
Temperature, pulse, and blood pressure show how sick the patient is and help spot dehydration or sepsis risk. MSD Manuals
Neck and jaw lymph node palpation
Tender, enlarged nodes support an active infection in the mouth and help track spread. Wikipedia
Assessment of mouth opening (trismus) and speech
Limited opening and muffled speech suggest deeper tissue or muscle involvement and higher severity. NCBI

B) Manual dental tests (simple chairside maneuvers)

Periodontal probing around involved teeth
Gentle probing checks attachment loss. Loss suggests necrotizing periodontitis or involvement beyond the gums. NCBI
Tooth mobility grading
Mobility implies ligament and bone injury from the necrotizing process. NCBI
Percussion sensitivity
Tapping teeth helps detect periapical irritation or bone involvement. Increased tenderness hints at deeper spread. NCBI
Palpation of mucosa and vestibule
Gentle pressure identifies fluctuance, crepitus, or extension into the cheek or floor of mouth. This helps map the true borders of the lesion. NCBI
Oral hygiene and plaque scoring
High plaque burden supports the clinical picture and guides prevention planning after the acute phase. NCBI

C) Laboratory and pathological tests

Complete blood count (CBC) with differential
Looks for anemia, leukocytosis, or neutropenia. Abnormal results show systemic impact and may uncover immune problems. NCBI
C-reactive protein (CRP) and ESR
Inflammation markers help grade severity and monitor response to treatment. NCBI
Serum albumin and basic metabolic panel
Low albumin and electrolyte issues point to malnutrition and dehydration, common cofactors in severe disease. World Health Organization
HIV testing (where appropriate and consented)
Because immunosuppression greatly increases risk and severity, testing helps guide care and prevention. NCBI
Blood glucose (screen for diabetes)
Hyperglycemia impairs wound healing and infection control; it is useful to check in stubborn cases. NCBI
Microbiology of ulcer swab (aerobic/anaerobic culture or 16S PCR)
Cultures often show mixed anaerobes. Although no single pathogen defines NUS, results can guide antibiotic choice in complicated cases. NCBI
Malaria or measles testing (context-specific)
Where endemic or suspected, tests identify intercurrent infections that worsen NUS risk and outcomes. World Health Organization

D) Electrodiagnostic and chairside physiologic tests (adjuncts)

Electric pulp testing of adjacent teeth
Checks vitality of teeth near necrotic areas. Loss of response may reflect deeper spread or secondary pulpal injury. (Adjunct test used in dental practice when bone extension is suspected.) NCBI
Pulse oximetry and hydration assessment
Simple noninvasive monitoring detects hypoxia or systemic compromise in febrile, dehydrated, or septic patients. Helpful for triage and safety. MSD Manuals

E) Imaging tests

Dental radiographs and cross-sectional imaging (tailored to severity)

Periapical and bitewing radiographs can show early bone changes around teeth.
Orthopantomogram (panoramic X-ray) surveys both jaws for bone loss or sequestra.
Cone-beam CT (CBCT) or CT/MRI of the face defines soft-tissue spread, abscesses, and osteonecrosis when NUS is extensive or complications are suspected. Imaging is chosen based on clinical severity and availability. aap.onlinelibrary.wiley.com

Non-pharmacological treatments (therapies & other care)

Urgent gentle oral cleaning — Purpose: reduce germs and dead tissue. Mechanism: frequent rinsing (saline; very dilute hydrogen peroxide when appropriate) loosens debris and lowers bacterial load so the body and antibiotics work better. Do not scrub hard; dab and rinse to avoid bleeding. www3.paho.org
Nutritional rehabilitation (high-calorie, high-protein diet) — Purpose: restore strength and immunity. Mechanism: protein, calories, and micronutrients support white-blood-cell function, collagen production, and wound closure; without nutrition the infection relapses. PubMed Central+1
Vitamin and micronutrient repletion — Purpose: correct common deficits (A, D, B-complex, iron, zinc). Mechanism: vitamins and minerals help epithelial repair, immune signaling, and bone turnover; WHO specifically directs vitamin A during severe acute malnutrition in children. World Health Organization+1
Hydration & electrolyte support — Purpose: prevent dehydration from pain-limited intake. Mechanism: fluids maintain perfusion to infected tissues and support antibiotic delivery and wound healing. PubMed Central
Local wound care/debridement by clinician — Purpose: remove clearly dead tissue while sparing viable mucosa. Mechanism: careful bedside debridement reduces anaerobic biomass and improves oxygenation at the wound edge. Hopkins Guides
Professional plaque control (scaling/root planing when tolerated) — Purpose: clean plaque and calculus that feed the infection. Mechanism: mechanical biofilm removal lowers pathogen counts and inflammation. NCBI
Oral hygiene instruction for caregivers — Purpose: maintain a clean mouth during healing. Mechanism: correct brushing/swabbing technique, safe rinses, and frequency reduce reinfection. ennonline.net
Analgesia with cold/warm compresses and paced eating — Purpose: improve pain so the patient can eat and drink. Mechanism: temperature therapy reduces local inflammation, enabling oral intake and medication adherence. NCBI
Isolation of necrotic areas from trauma — Purpose: protect ulcers from tooth edges or hot/spicy foods. Mechanism: minimizing friction and chemical irritation reduces bleeding and helps re-epithelialization. DermNet®
Psychosocial support — Purpose: reduce stress that worsens periodontal disease and improves adherence. Mechanism: caregiver education and counseling help maintain hygiene and nutrition routines. NCBI
Management of contributing illnesses (e.g., HIV, measles, other infections) — Purpose: fix the root causes that suppress immunity. Mechanism: treating co-infections lowers the risk of spread or relapse. World Health Organization+1
Probiotic oral adjuncts (lozenges/yogurt; clinician-approved) — Purpose: help rebalance the mouth microbiome after cleaning. Mechanism: certain strains compete with pathogens and may reduce plaque and halitosis; these are adjuncts, not replacements for care. PubMed Central+1
Smoking cessation (if applicable) — Purpose: speed healing. Mechanism: tobacco impairs blood flow and immune cell function in gums. NCBI
Safe chlorhexidine mouth-rinsing protocol (short course) — Purpose: reduce plaque bacteria. Mechanism: chlorhexidine binds to oral surfaces and disrupts bacterial membranes. Use as directed by a clinician to limit staining/altered taste. FDA Access Data+1
Warm saline rinses after meals — Purpose: gentle cleaning and comfort. Mechanism: hypertonic saline draws fluid from swollen tissue and dislodges debris without trauma. ennonline.net
Positioning & trismus prevention exercises (when pain permits) — Purpose: keep mouth opening and prevent scarring/lock-jaw. Mechanism: gentle range-of-motion and jaw physiotherapy preserve function during healing. Semantic Scholar
Early recognition education for families — Purpose: detect recurrence or spread quickly. Mechanism: teaching “red flags” (sudden gum pain, gray film, fever, face swelling) prompts rapid care. www3.paho.org
Infection control in community settings — Purpose: lower transmission of general infections that precipitate noma. Mechanism: basic hygiene, safe water, and vaccination outreach reduce triggers like measles. World Health Organization
Follow-up maintenance program — Purpose: stop relapse. Mechanism: routine checks for hygiene, nutrition, and soft-tissue healing catch problems early. NCBI
Referral pathway for reconstructive planning (after the acute phase) — Purpose: restore chewing, speech, and appearance after large defects. Mechanism: staged planning with maxillofacial teams improves quality of life. SAGE Journals+1

Drug treatments

Doses are typical adult starting points unless noted; clinicians tailor to age, weight, severity, and local resistance. Always combine with local care and nutrition.

Penicillin G (benzathine or parenteral penicillin G sodium/potassium) — Class: beta-lactam. Dose/time: e.g., Penicillin G potassium IV in divided doses per label; benzathine penicillin IM for specific indications. Purpose: cover oral streptococci and other susceptible aerobes common early in disease. Mechanism: inhibits cell-wall synthesis. Side effects: allergy, injection-site pain, rare neurotoxicity at very high doses. FDA Access Data+2FDA Access Data+2
Metronidazole — Class: nitroimidazole anti-anaerobe. Dose: 500 mg PO/IV q8–12h (adult) per label. Purpose: target anaerobes (e.g., Fusobacterium/Prevotella) that drive necrosis and halitosis. Mechanism: DNA strand breakage under anaerobic conditions. Side effects: metallic taste, GI upset, disulfiram-like reaction with alcohol. FDA Access Data+1
Amoxicillin-clavulanate (Augmentin) — Class: aminopenicillin + beta-lactamase inhibitor. Dose: per label (e.g., 875/125 mg PO q12h). Purpose: broaden gram-negative/anaerobe coverage when mixed flora is suspected. Mechanism: amoxicillin blocks cell wall; clavulanate protects against beta-lactamases. Side effects: diarrhea, rash, rare hepatic enzyme increase. FDA Access Data
Clindamycin — Class: lincosamide. Dose: 300 mg PO q6–8h or IV per label. Purpose: alternative for severe penicillin allergy, good anaerobic and streptococcal coverage. Mechanism: inhibits 50S ribosome. Side effects: risk of C. difficile colitis; rash. FDA Access Data+1
Ceftriaxone (adjunct in severe facial cellulitis/sepsis) — Class: 3rd-gen cephalosporin. Dose: per institutional protocol. Purpose: broad gram-negative/streptococcal coverage with IV once-daily dosing in complicated cases. Mechanism: cell-wall inhibition. Side effects: biliary sludging, allergy. (Use guided by local practice; not every case needs this.) Hopkins Guides
Chlorhexidine 0.12% oral rinse (Peridex) — Class: antiseptic mouthwash (topical). Dose: 15 mL swish/spit BID short course as directed. Purpose: plaque control during acute care. Mechanism: cationic membrane disruption. Side effects: tooth staining, altered taste if prolonged. FDA Access Data+1
Ibuprofen — Class: NSAID analgesic. Dose: OTC 200–400 mg PO q6–8h PRN within label limits. Purpose: reduce pain and fever so the patient can drink/eat. Mechanism: COX inhibition lowers prostaglandins. Side effects: GI irritation, kidney risk, CV warnings at higher/longer use. FDA Access Data+1
Acetaminophen (paracetamol) — Class: analgesic/antipyretic. Dose: per label total daily max (consider all sources). Purpose: pain/fever control when NSAIDs are unsuitable. Mechanism: central prostaglandin effect. Side effects: liver toxicity if overdosed. FDA Access Data
Lidocaine 2% viscous (topical) — Class: local anesthetic. Dose: small measured swish or dab to painful mucosa as directed. Purpose: short-term numbing to allow oral intake and oral care. Mechanism: sodium-channel blockade in mucosa. Side effects: numb tongue/throat, aspiration risk if overused; systemic toxicity if excessive. FDA Access Data
Nystatin oral suspension (if secondary candidiasis) — Class: polyene antifungal (topical oral). Dose: swish and swallow/swish and spit per label. Purpose: treat oral thrush that can follow broad antibiotics and malnutrition. Mechanism: binds ergosterol, pores in fungal membrane. Side effects: GI upset. FDA Access Data+1
Fluconazole (for candidiasis not responding to topical therapy) — Class: triazole antifungal (systemic). Dose: per label and clinician judgement. Purpose: step-up therapy for moderate oral candidiasis. Mechanism: inhibits fungal ergosterol synthesis. Side effects: hepatic enzyme elevation, drug interactions. FDA Access Data
Penicillin G benzathine (IM) for specific scenarios per clinician — Class: long-acting penicillin. Dose: IM per label. Purpose: when adherence is uncertain and streptococcal coverage is needed in selected settings. Mechanism: prolonged low-level beta-lactam exposure. Side effects: injection pain, allergy. FDA Access Data
Amoxicillin (plain), where beta-lactamase risk is low — Class: aminopenicillin. Dose: per local protocol. Purpose: simpler regimen in early gingival necrosis with low resistance. Mechanism: cell-wall inhibition. Side effects: rash, GI upset. www3.paho.org
Combination penicillin + metronidazole (empiric) — Class: beta-lactam + anti-anaerobe. Dose: per above components. Purpose: common empiric duo to cover predominant noma pathogens when severe. Mechanism: dual aerobic/anaerobic cover. Side effects: as above; avoid alcohol with metronidazole. Hopkins Guides+1
Clindamycin + metronidazole (penicillin-allergic severe cases) — Class: lincosamide + nitroimidazole. Dose: per labels. Purpose: broad anaerobic and gram-positive coverage when penicillin cannot be used. Mechanism: protein synthesis + DNA damage. Side effects: C. difficile risk; GI upset. FDA Access Data+1
Topical povidone-iodine (clinician-directed) — Class: antiseptic. Use: diluted topical cleansing in procedures. Purpose: reduce surface bioburden. Mechanism: iodination/oxidation of proteins. Side effects: staining, iodine sensitivity. joooo.org
Oral rehydration solution (ORS) — Class: electrolyte solution. Dose: frequent small sips. Purpose: correct dehydration that worsens tissue perfusion. Mechanism: glucose-sodium cotransport enhances water absorption. PubMed Central
Antipyretic rotation (acetaminophen/ibuprofen per label) — Class: analgesics. Purpose: reduce fever-pain cycle that blocks eating and oral care. Mechanism: central/peripheral prostaglandin effects. Side effects: as above; avoid overdose. FDA Access Data+1
Antiseptic saline/hydrogen-peroxide mouth care (dilute, time-limited) — Class: local antiseptic. Use: clinician-guided in early acute care. Purpose: decrease anaerobic load and clean debris. Mechanism: osmotic effect / oxygen release. www3.paho.org
Antibiotic step-down to oral agents after stabilization — Class: per above choices. Purpose: finish a full, appropriate course after IV therapy and clinical improvement. Mechanism: sustained suppression of pathogens until mucosa heals. Side effects: drug-specific. (Evidence comparing exact regimens is limited.) BMJ Global Health

Dietary molecular supplements

Vitamin A (with SAM protocols in children) — Supports epithelial repair and immune function; WHO provides specific dosing within severe acute malnutrition programs. World Health Organization
Vitamin D — Low vitamin D is linked with worse periodontal status; adjunct repletion may aid periodontal therapy (evidence evolving). PubMed Central+1
B-complex (especially folate, B12) — Needed for cell division and mucosal repair; deficiency worsens oral ulcers. PubMed Central
Protein supplements (milk/legume powders) — Provide amino acids for collagen and immune proteins when chewing is painful. PubMed Central
Zinc (only if deficient) — Mixed evidence; helpful mainly when deficiency exists; not a universal wound-healing cure. Cochrane+1
Iron (if iron-deficiency anemia) — Reverses anemia that impairs immunity and healing; use after testing. PubMed Central
Probiotic foods (yogurt/kefir) or clinician-approved lozenges — May reduce plaque/halitosis as an adjunct. PubMed Central
Omega-3 fatty acids (food-first) — Anti-inflammatory support for periodontal tissues (adjunctive, not primary therapy). PubMed Central
Vitamin C — Supports collagen cross-linking and gingival healing in deficiency states. PubMed Central
Multimicronutrient powders for children (per programs) — Practical way to correct multiple deficits in high-risk settings. World Health Organization

Immunity-support / regenerative” drug domains

Antibiotics started early — They are the most effective “immune support” because they remove the bacterial burden the immune system cannot handle alone in malnourished patients. Hopkins Guides
Vaccination (measles and other EPI vaccines) — Prevents infections that precipitate noma in children; strengthens population immunity. World Health Organization
Micronutrient repletion (A, D, iron, zinc if low) — Restores innate and adaptive immune responses required to control oral bacteria. World Health Organization+1
Analgesia enabling intake — Pain control is “regenerative” in practice because it allows nutrition and sleep, which drive tissue repair. FDA Access Data+1
Antifungals when needed — Clearing thrush removes a secondary barrier to eating and oral care in antibiotic-treated, malnourished mouths. FDA Access Data
Reconstructive surgery in the sequelae phase — Restores oral competence so patients can chew, speak, and maintain hygiene, preventing recurrent infections. SAGE Journals+1

Surgeries (what they are and why done)

Acute conservative debridement — Remove only clearly dead tissue to control odor and contamination; definitive reconstruction waits until the infection is quiet. Hopkins Guides
Sequestrectomy / debridement of necrotic bone — Take out loose dead bone to stop chronic infection and allow granulation. NCBI
Release of trismus / scar bands — Restore mouth opening for eating, speech, and hygiene after healing. Semantic Scholar
Local or regional flap reconstruction (e.g., submental, deltopectoral) — Replace missing cheek/lip mucosa and skin; widely used with good functional results in resource-limited settings. cdn.fortunejournals.com+1
Staged comprehensive reconstruction — In specialized centers, planned multi-stage repairs (sometimes microvascular) improve function and quality of life. SAGE Journals+1

Preventions

Good daily oral hygiene and routine dental care. NCBI
Adequate nutrition and safe water for children. World Health Organization
Early care for gingival pain, bleeding, or gray film on the gums. www3.paho.org
Vaccinations (especially measles). World Health Organization
Prompt antibiotics for confirmed necrotizing gingivitis/stomatitis in high-risk settings. ennonline.net
Treat HIV and other immune-weakening conditions. World Health Organization
Tobacco cessation. NCBI
Caregiver education on early signs and mouth care. www3.paho.org
Follow-up maintenance after recovery. NCBI
Community awareness to reduce stigma and delays in care. PubMed Central

When to see a doctor urgently

Seek urgent care the same day if there is sudden mouth pain with gray-white tissue, bad breath, bleeding gums that hurt to touch, fever, jaw or cheek swelling, difficulty opening the mouth, or if the person is a malnourished child or an immunocompromised adult. Early care stops the disease and prevents noma; delays raise the risk of tissue loss and death. NCBI+1

What to eat and what to avoid (during healing)

Choose soft, high-protein, high-calorie meals (eggs, milk, lentils, yogurt, blended soups), plenty of safe fluids, and vitamin-rich fruits/vegetables as tolerated. Avoid sharp, spicy, very hot, or acidic foods that sting the ulcers; avoid alcohol and tobacco. If chewing is hard, use purees and fortified porridges; small, frequent meals help. These steps make antibiotics and local care more effective by restoring immune function. PubMed Central

FAQs

Is it contagious? — It is a polymicrobial infection that thrives when the body is weak; improving nutrition and hygiene and giving antibiotics controls it. NCBI
Who gets severe disease (noma)? — Mostly malnourished children 2–6 years old; can occur in immunocompromised adults. World Health Organization
How fast does it spread? — Hours to days without care; early care halts it. www3.paho.org
Why does the breath smell foul? — Anaerobic bacteria produce volatile sulfur compounds. Metronidazole helps by killing anaerobes. FDA Access Data
Do I always need antibiotics? — Yes for necrotizing stomatitis; regimen often includes penicillin-class plus metronidazole unless allergic. Hopkins Guides
Can mouthwash alone cure it? — No. Antiseptics are adjuncts only. FDA Access Data
What imaging is used if bone is suspected? — CT (and sometimes MRI) defines bone death and deep space spread. NCBI+1
Will teeth be lost? — Possibly, if bone and ligament are destroyed; early care lowers this risk. NCBI
Are probiotics helpful? — As add-ons they may help plaque/halitosis, but they do not replace antibiotics or cleaning. PubMed Central
Does vitamin D matter? — Low levels are linked with worse periodontal disease; correcting deficiency may help therapy. PubMed Central
Is there a single “best” antibiotic regimen? — Evidence is limited; most experts pair a penicillin with metronidazole and tailor to the patient. BMJ Global Health+1
When is surgery done? — Minimal debridement in the acute stage; reconstruction after months when the disease is quiet. SAGE Journals
How do we prevent relapse? — Maintenance hygiene, nutrition, treatment of underlying disease, and follow-up. NCBI
Is it rare? — Severe noma is rare but devastating in extremely poor settings; early necrotizing gum disease is more common. World Health Organization
What is the single most important action? — Start treatment early: antibiotics + nutrition + gentle oral care. Hopkins Guides+1

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