Causes

• Volatile sulfur compounds: H₂S, methyl mercaptan, dimethyl sulfide

Detection Methods

• Gold standard: Organoleptic rating (easiest)
• Most sensitive: Gas chromatography

Necrotizing Ulcerative Gingivitis (NUG)

Necrotizing Ulcerative Gingivitis (NUG), also known as Vincent's disease or trench mouth, is a severe form of periodontal disease characterized by the sudden onset of symptoms and specific clinical features.

Etiology and Predisposing Factors

• Sudden Onset: NUG is characterized by a rapid onset of symptoms, often following debilitating diseases or acute respiratory infections.
• Lifestyle Factors: Changes in living habits, such as prolonged work without adequate rest, poor nutrition, tobacco use, and psychological stress, are frequently noted in patient histories .
• Smoking: Smoking has been identified as a significant predisposing factor for NUG/NDP .
• Immune Compromise: Conditions that compromise the immune system, such as poor oral hygiene, smoking, and emotional stress, are major contributors to the development of NUG .

Clinical Presentation

• Symptoms: NUG presents with:
  • Punched-out, crater-like depressions at the crest of interdental papillae.
  • Marginal gingival involvement, with rare extension to attached gingiva and oral mucosa.
  • Grey, pseudomembranous slough covering the lesions.
  • Spontaneous bleeding upon slight stimulation of the gingiva.
  • Fetid odor and increased salivation.

Microbiology

• Mixed Bacterial Infection: NUG is caused by a complex of anaerobic bacteria, often referred to as the fusospirochetal complex, which includes:
  • Treponema vincentii
  • Treponema denticola
  • Treponema macrodentium
  • Fusobacterium nucleatum
  • Prevotella intermedia
  • Porphyromonas gingivalis

Treatment

1. Control of Acute Phase:

   • Clean the wound with an antibacterial agent.
   • Irrigate the lesion with warm water and 5% vol/vol hydrogen peroxide.
   • Prescribe oxygen-releasing mouthwash (e.g., hydrogen peroxide DPF, sodium perborate DPF) to be used thrice daily.
   • Administer oral metronidazole for 3 to 5 days. If sensitive to metronidazole, prescribe penicillin; if sensitive to both, consider erythromycin or clindamycin.
   • Use 2% chlorhexidine in select cases for a short duration.

2. Management of Residual Condition:

   • Remove predisposing local factors (e.g., overhangs).
   • Perform supra- and subgingival scaling.
   • Consider gingivoplasty to correct any residual gingival deformities.

Pathophysiology

• Enzyme defect: Glucose-6-phosphate dehydrogenase deficiency
• Result: Impaired NADPH production → reduced glutathione → oxidative damage
• Inheritance: X-linked recessive (affects males predominantly)

Key Clinical Features

• Heinz bodies: Characteristic finding (precipitated denatured hemoglobin)
• Hemolytic episodes: Triggered by oxidative stress
• Chronic hemolysis: Usually absent between episodes
• Neonatal jaundice: May be severe

Important Clinical Points

• Estrogen does NOT induce hemolysis (unlike other conditions)
• Favism: Hemolysis after eating fava beans
• Drug-induced: Most common trigger for hemolytic crisis

Oxidative Stressors to Avoid

Medications

• Antimalarials: Primaquine, chloroquine
• Antibiotics: Sulfonamides, nitrofurantoin, chloramphenicol
• Analgesics: Aspirin (high doses), phenazopyridine
• Others: Methylene blue, naphthalene (mothballs)

Infections

• Bacterial infections
• Viral hepatitis
• Pneumonia
• Typhoid fever

Other Triggers

• Fava beans (favism)
• Diabetic ketoacidosis
• Severe illness/stress

Periodontics: Dental specialty deals with the supporting and surrounding tissues of the teeth. 

1. Periodontium: tissues that invest and support teeth Includes Gingiva, Alveolar mucosa  Cementum, Periodontal ligament, Alveolar bone, Support bone

2. Periodontal disease: changes to periodontium beyond normal range of variation

a. Specific plaque hypothesis: specific microorganisms cause periodontal disease; mostly anaerobes. Three implicated: Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Bacteriodes forsythus

b. Contributing factors: often a combination of factors

i. Local: calculus (tarter, home for bacteria, ­ with age), traumatic occlusal forces, caries (root caries), overhangs and over-contoured restorations, open contacts with food impaction, missing/malaligned teeth

Invasion of biological width: from free gingival margin -> attached gingiva need ~ 3 mm.  If enter this area -> problems (e.g., resorption)

ii. Host factors: exacerbate periodontal problems; e.g., smoking/tobacco use, pregnancy and puberty (hormonal changes, ­ blood vessel permeability), stress, poor diet

iii.Medications: often -> tissue overgrowth; e.g., oral contraceptives, antidepressants, heart medicines, transplant anti-rejection drugs

iv.Systemic diseases: e.g., diabetes, immunosuppression

B. Gingivitis: inflammation of gingiva; ­ with age; generally reversible

C. Periodontitis: inflammation of supporting tissues of teeth, characterized by loss of attachment (PDL) and bone; generally irreversible

D.       Periodontal disease as risk factor for systemic diseases:

1.        Causes difficulty for diabetics to control blood sugar

2.        Pregnant women with periodontal disease ~ 7 times more likely to have premature and/or underweight baby

3.        Periodontal diseased patients may be at risk for heart disease

🔻 Anemia Types

🔸 Microcytic

🔸 Macrocytic

• Pernicious anemia: ↓ intrinsic factor
• MCH ↑, MCHC normal
• Hypokalemia during treatment
• Causes: Dietary folate deficiency, celiac disease
• Thiamine deficiency → Lactic acidosis

🔸 Sideroblastic

• Causes: Hypothyroidism, INH therapy
• Treatment: Pyridoxine
• Genetic variant: Pearson syndrome

• Papillon-Lefevre Syndrome: Periodontitis, hyperkeratosis, dural calcification.
• Chediak-Higashi Disease: Neutrophil function defect.
• Iron Deficiency Anemia: Moderate bone loss with periodontitis.