Index
This disease manifests in both acute and recurrent phases.
Vincent’s angina was named for the French physician Henri Vincent (1862-1950). This condition is also known as necrotizing ulcerative gingivitis; it is a common type of gingivitis.
This inflammatory condition primarily involves the free gingival margin, the gingiva ridge, and the interdental papillae. When the lesions extend to the soft palate and tonsillar areas, Vincent’s angina applies.
The word “angina” is derived from the Latin word “anger,” which means “to choke or strangle.”
Other names for this condition are:
- Necrotizing ulcerative gingivitis.
- Vincent’s infection.
- Ditch mouth.
- Acute ulceromembranous gingivitis.
- Phagedenic gingivitis.
- Fusospirochetal gingivitis.
- Acute ulcerative gingivitis.
The short form of acute necrotizing ulcerative gingivitis is ANUG. Acute necrotizing ulcerative gingivitis occurs in an epidemic pattern, sweeping through groups of people in close contact, especially those living in similar conditions.
Word of mouth from the trench originates because the disease was especially prevalent among troops in the tracks during World War I. Similar sporadic outbreaks also occurred during WWII.
Although this condition is rare in developed countries, there has been a global increase associated with HIV infection.
In many cases, the pattern of spread of the disease indicated that it was a contagious infection, but this is not accepted now.
It occurs in groups of people that can be explained based on similar predisposing conditions among group members, which can cause gingivitis to develop in each of them, even though there is no actual contact between them.
Vincent’s angina can occur at any age but is reported to be most common among young and middle-aged adults, ages 15 to 35. It is seen almost exclusively in children in developing countries, linked to poverty and malnutrition.
What are the causes of Vincent’s angina?
It is an endogenous, polymicrobial infection that causes destructive inflammation due to the coexistence of several predisposing factors. It is caused by a spindle-shaped bacillus and a borrelia Vicentina spirochete.
These organisms may be present in small amounts in healthy gingival flora.
Both microorganisms dominate in this fusospirochetal disease, although other spirochetes, fusiform, and filamentous organisms are also found.
Several factors likely disrupt the host-parasite relationship, facilitating the overgrowth of the organisms of the fusospirochetal complex.
Cause of recurrence of necrotizing ulcerative gingivitis
After necrotizing ulcerative gingivitis heals, the ridges of the beds, which have been destroyed, leaving a hollowed-out area, constitute an area that retains debris and microorganisms and can serve as an incubation zone.
This area, along with the gingival flaps of the erupting third molars, is an ideal place for the organisms to persist, and, in many cases, the recurrence of necrotizing ulcerative gingivitis will begin here.
Gum smears of necrotizing ulcerative gingivitis show large numbers of spindle-shaped bacilli and an oral spirochete, other spirochetes, filamentous organisms, vibrios, cocci, desquamated epithelial cells, and a variable number of polymorphonuclear leukocytes.
The relative number of microorganisms present varies with the stage of the disease.
What are the risk factors for Vincent’s angina?
Stress psychology plays a vital role in the development of angina Vincent, as there is a higher frequency of the disease in people in the military.
Other predisposing factors include immunosuppression, smoking, upper respiratory infection, local trauma, poor nutritional status, and poor oral hygiene.
HIV-positive people develop a severe form of necrotizing ulcerative gingivitis as immune function deteriorates, which progresses to HIV-associated periodontitis.
Decreased resistance to infection is one of the most important predisposing factors in developing necrotizing ulcerative gingivitis.
What are the symptoms of Vincent’s angina?
The disease is characterized by the development of painful and hyperemic gingiva and an acutely expelled crater, such as erosions of the interdental papillae and bleeding of the free gingiva when touched. It is usually covered with a grayish-green necrotic pseudomembrane.
Ulceration tends to spread and may eventually affect all gingival margins.
It commonly starts from a single isolated bulb with a quick start.
Ultimately, a foul odor develops that is highly unpleasant.
The patient almost always complains of an inability to eat due to severe gingival pain and a tendency to gingival bleeding.
The pain is that of external pressure. The patient generally suffers from headaches, malaise, and low-grade fever.
Excessive salivation is often observed with a metallic taste to saliva. Regional lymphadenopathy is usually present.
In advanced and more severe cases, there may be generalized or systemic manifestations, including leukocytes, gastrointestinal disturbances, and tachycardia.
What is the treatment for this condition?
Treatment of necrotizing ulcerative gingivitis is highly varied, depending on the individual dentists’ experience with the disease.
Some prefer to treat this condition conservatively and institute only superficial cleaning of the oral cavity in the early acute stage of the disease with chlorhexidine, dilute hydrogen peroxide, or warm saline water.
A wide-scale and polish follow this. Topical anesthesia may require reducing pain during this procedure.
Antibiotics are also recommended along with local treatment. The usual case of necrotizing ulcerative gingivitis begins to diminish within 48 hours with adequate treatment, and there may be little evidence after the presence of the disease.
