• Gingivitis - Causes and treatments

Common causes: 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 actinomycetemcomitans and Porphyromonas gingivalis)

Description

  • Very common condition characterized by painless inflammation of the gingivae, erythema, bleeding while brushing the teeth, edema, and often recession of the gingivae
  • Most common form is chronic plaque-associated nonspecific inflammation caused by polymicrobial infection
  • Represents first stage of periodontal disease (loss of alveolar bone) but is reversible if treated

Cardinal features:

  • Inflammation of the gums is usually painless unless in a progressive form of the disease (acute necrotizing ulcerative gingivitis)
  • Bleeding of the gums with minor trauma (such as from brushing the teeth)
  • Reddened gums
  • Halitosis
  • Presence of subgingival plaque

Forms:

  • Acute necrotizing ulcerative gingivitis (acute infection of the gingivae):
  • Edematous interdental papillae
  • Crateriform lesions, most commonly in the anterior incisor and posterior molar regions
  • Erythema
  • Spontaneous gingival hemorrhage
  • Necrosis with formation of a grayish pseudomembrane over affected area
  • Pain with rapid onset
  • Halitosis
  • Blunted gingivae between the teeth (normally cone-shaped)
  • Often accompanied by fever, malaise, and lymphadenopathy
  • Often associated with immunosuppression, 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 communicable
  • Vincent angina (the spread of acute necrotizing ulcerative gingivitis to the adjacent oropharynx):
  • Membranous pharyngitis
  • Painful ulceration on the gingivae, buccal mucosa, and pharynx with hyperemic patches
  • Edema
  • Fever
  • Swelling of lower face and neck
  • Difficulty with speech or swallowing
  • Rapid progression (hours to days)
  • Drug-induced gingival hyperplasia:
  • An adverse effect of corticosteroids, phenytoin, cyclosporine, and nifedipine (switching from nifedipine to isradipine may help)
  • Generalized hyperplasia of the gingivae, resulting from fibrous tissue overgrowth
  • Includes the features of 'ordinary' gingivitis

Epidemiology

Frequency

  • Among adults, 50% to 90% have gingivitis (surrounding 3 or 4 teeth)
  • Only up to 13% of the population is susceptible to severe periodontal disease

Demographics

Age:

  • In children: Almost all children will have gingivitis at one time or another (surrounding at least 1 tooth). However, since young children do not usually harbor Actinobacillus actinomycetemcomitans or Porphyromonas gingivalis, they are at low risk of severe periodontal disease. Usually no treatment is necessary
  • In adults: The incidence of gingivitis increases with age, peaking at around age 34
  • In the elderly: High incidence of gingivitis—in those with their own teeth there is a cumulative effect because of age; those who wear dentures are prone to gingivitis from ill-fitting prostheses

Gender:

  • Prevalence is generally equal between the sexes. However, women can be more susceptible owing to hormonal influences, and men owing to typically poorer hygiene habits

Race:

  • Generally pandemic; however, African Americans have a higher incidence than Caucasians, who in turn have a higher incidence than Hispanics

Genetics:

  • No genetic factor for gingivitis; however, studies show that children of parents with periodontal disease are more likely to have oral bacteria responsible for plaque
  • There may be genetic susceptibility to periodontal disease, although other factors are also responsible. Research suggests that Porphyromonas gingivalis may be contagious and transmissible after extended exposure to an infected person

Socioeconomic status:

  • Lower socioeconomic groups may not have access to dental care or be aware of preventive measures

Causes and risk factors

Common causes

  • 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 actinomycetemcomitans andPorphyromonas 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 saliva
  • Vitamin deficiency, especially of vitamin C

Rare causes

  • Hormonal fluctuations during pregnancy (because of increased levels of progesterone, which dilate blood vessels and block collagen repair), adolescence, or menopause (menopausal gingivostomatitis is characterized by dry, shiny gums that bleed easily, accompanied by odd tastes and sensations in the mouth)
  • Reaction to oral contraceptives
  • Gingival hyperplasia caused by medications (can be an adverse effect of corticosteroids, phenytoin, cyclosporine, and nifedipine)
  • Leukemia and other rare blood disorders
  • Systemic causes: metabolic disorders such as thyroid disorders or diabetes (type 1 or type 2—if improperly controlled there may be an increase in levels of triglycerides and interleukins, which influence the inflammatory response that underlies periodontal disease), nutrient deficiencies, or HIV infection

Risk factors

  • Poor oral hygiene
  • Malocclusion that results in inaccessibility for brushing and flossing
  • Premenstrual hormonal changes: gingivitis flare-ups just before onset of menstruation
  • Obesity: some studies indicate that obesity may predispose to gum disease
  • Down syndrome: because of increased sensitivity to inflammatory process

Malnutrition: studies have shown a trend to less plaque and gingivitis in well-nourished versus malnourished people

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