Vincent Stomatitis

BASICS

An inflammatory infection of the gingiva, characterized by pain, ulcerations, and necrotizing damage to interdental papillae

DESCRIPTION

  • Caused by an imbalance of oral flora, resulting in a predominance of anaerobic bacteria that invade the gingival mucosa and form a gray pseudomembranous exudate
  • Clinical presentation includes oral pain, fetid breath, gingival ulcerations, necrosis, and bleeding
  • Whereas other periodontal diseases develop over time, necrotizing periodontal disease is characterized by its rapid onset, pain, ulcerated gingival mucosa, and “punched out” crater-like lesions of interdental papillae (1).
  • The most common bacteria include Fusobacterium spp., Prevotella intermedia, and spirochetes. Concomitant infection with Epstein-Barr virus, herpes simplex virus, and type 1 human cytomegalovirus is common.
  • Synonym(s): Vincent angina; Vincent disease; Vincent stomatitis, trench mouth; fusospirochetal gingivitis; acute necrotizing ulcerative gingivitis (ANUG); necrotizing ulcerative gingivitis (NUG)
  • Necrotizing gingivitis, necrotizing periodontitis, and necrotizing stomatitis are classified together under the umbrella term “necrotizing periodontal disease (NPD).”

EPIDEMIOLOGY

Colloquially called “trench mouth,” necrotizing periodontal disease predominantly affects younger populations with poor oral hygiene and inadequate nutrition.

Incidence

  • Predominant age: 18 to 30 years in developed countries, malnourished children ages 3 to 14 years
  • Affects both genders with similar frequency
  • Historically, incidence increased in military personnel due to poor battlefield conditions and psychological stress, hence the use of the informal phrase, “trench mouth” (1).

Prevalence

  • The true prevalence is unknown, but likely <1% overall (1).
  • Worldwide prevalence has declined since World War II (1).
  • A rare disease in developed countries; however, recent data demonstrated a prevalence rate of 6.7% in Chilean students between 12 and 21 years and approaching 25% in children in sub-Saharan African countries (2),(3).

ETIOLOGY AND PATHOPHYSIOLOGY

  • Immunocompromised state resulting in poor host response to invasive anaerobic bacteria
  • Disruption of normal oral flora with a predominance of invasive anaerobic bacteria (Treponema spp., Selenomonas spp., Fusobacterium spp., and Prevotella intermedia) (2)
  • Invasive anaerobic bacteria produce metabolites such as collagenase, endotoxins, and fibrinolysin that destroy tissue, leading to loss of integrity and necrosis of the gingival mucosa and interdental papillae (4).
  • Stress increases adrenocortical hormones and reduces gingival microcirculation and salivary flow, which alters leukocyte and lymphocyte function. Stress may also result in behavioral changes that lead to poor oral hygiene and malnutrition (2).
  • Increased bacterial attachment with active herpesvirus infection

RISK FACTORS

  • Malnutrition
  • Immunosuppression (diabetes, alcohol use, HIV, cancer, chemotherapy, steroid use)
  • Low socioeconomic status
  • Tobacco use
  • Poor oral hygiene, infrequent or absent dental care
  • Orthodontics
  • Herpesvirus infection
  • Psychological stress

GENERAL PREVENTION

  • Appropriate nutrition
  • Proper oral hygiene
  • Regular dental care
  • Prompt recognition and institution of therapy
  • Management of medical problems such as cancer and HIV infection
  • Smoking cessation
  • Stress management

COMMONLY ASSOCIATED CONDITIONS

  • Most commonly seen in malnourished patients, patients undergoing cancer treatment, or those from underdeveloped countries
  • Bacteremia
  • Tooth loss
  • Chronic gingivitis
  • Noma (cancrum oris), a gangrenous infection of the oral mucosa
  • Aspiration pneumonia

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