Updated: Oct 15, 2008
Gingivitis is an inflammatory process limited to the mucosal epithelial tissue surrounding the cervical portion of the teeth and the alveolar processes. Gingivitis has been classified by clinical appearance (eg, ulcerative, hemorrhagic, necrotizing, purulent), etiology (eg, drug-induced, hormonal, nutritional, infectious, plaque-induced), and duration (acute, chronic). The most common type of gingivitis is a chronic form induced by plaque.
Acute necrotizing ulcerative gingivitis (ANUG, ie, trench mouth) is an acute infectious gingivitis. The term trench mouth was coined in World War I when ANUG was common among trench-bound soldiers.
The most common type of gingivitis involves the marginal gingiva and is brought on by the accumulation of microbial plaques in persons with inadequate oral hygiene. Gingivitis proceeds through an initial stage to produce early lesions, which then progress to advanced disease.
The initial stage of an acute exudative inflammatory response begins within 4 or 5 days of plaque accumulation. Both gingival fluid and transmigration of neutrophils increase. Deposition of fibrin and destruction of collagen can be noted in the initial stage. At approximately 1 week, transition to early lesions is marked by the change to predominately lymphocytic infiltrates. Monocytes and plasma cells also may be present. With time, lesions become chronic and are characterized by the presence of plasma cells and B lymphocytes. As chronic local inflammation progresses, pockets develop where the gingiva separates from the tooth. These pockets deepen and may bleed during tooth brushing, flossing, and even normal chewing. As this persistent inflammation continues, periodontal ligaments break down and destruction of the local alveolar bone occurs. Teeth loosen and eventually fall out.
ANUG is a completely different syndrome caused by acute infection of the gingiva with organisms such as Prevotella intermedia, alpha-hemolytic streptococci, Actinomyces species, or any of a number of different oral spirochetes. ANUG may result in accelerated destruction of affected tissues, as well as local or systemic spread of infection.
Noma (cancrum oris) is a syndrome in which ANUG spreads beyond the gingiva. The infection invades local tissues of the mouth and face.
Frequency is difficult to determine because of the lack of agreement on measurement criteria. Many people believe that gingivitis begins in early childhood and that 9-17% of children aged 3-11 years have gingivitis. At puberty, prevalence rises to 70-90%. In recent years, periodontal disease, the endpoint of chronic gingivitis, slowly has decreased among adult Americans.
ANUG may be a clinical problem in immunocompromised patients during chemotherapy. Gingivitis and resulting periodontal disease are seen more frequently in patients with either diabetes or HIV.
Studies in Australia, Sweden, England, and Switzerland report gingivitis in 48-85% of children aged 3-6 years, but whether this range reflects population differences or whether it is due to different criteria used to define the disease is difficult to know. In adolescence, incidence around the world is comparable to US data (70-90%). ANUG may be found in areas where those at risk, particularly children, face poor living conditions. Recent publications show several cases in areas such as Nigeria, where ANUG and noma were observed in children younger than 14 years.1
Periodontal disease has been shown in some studies to be an associated factor in coronary artery disease (CAD) and cerebrovascular disease/ischemic stroke.2,3,4 This association with CAD has not been shown in all studies. Periodontal disease in pregnancy has been associated with an increase in preterm birth.5 Periodontitis in a person with diabetes has been associated with exacerbation of both conditions.6,7
Historical findings depend on whether the patient has chronic gingivitis or ANUG.
Adrenal Insufficiency and Adrenal Crisis
HIV Infection and AIDS
Gingivitis, desquamative
Gingivitis, diabetes mellitus
Gingivitis, phenytoin
Gingivitis, pregnancy
Glossitis
Noma (cancrum oris)
Pericoronitis
Periodontitis
Vincent angina (trench mouth)
In chronic gingivitis, brushing with a fluoride dentifrice will slow disease progression and may help resolution. Most electric toothbrushes have additional benefit over manual brushing. Daily flossing in addition to brushing will reduce plaque and bacterial counts. Recent studies show that brushing followed by rinsing with chlorhexidine or other solutions may have even better results over brushing and flossing.8,9 Gum-care–specific preparations that show benefit are available.10 Nonsteroidal anti-inflammatory drugs (NSAIDs) have been shown to speed the resolution of inflammation when teeth are being cleaned and scaled to remove plaque.11,12
In patients with ANUG, treatment involves antibiotics, NSAIDs, and topical Xylocaine for pain relief. Saline rinses can help to speed resolution, and oral rinses with a hydrogen peroxide 3% solution also may be of benefit.
These agents are used to eradicate the bacterial infection that is the hallmark of ANUG. In the future, antibiotics also may be used to treat simple chronic gingivitis, but no current evidence exists to justify this practice. Treatment of gingivitis may be warranted if dental surgery is planned.
DOC in patients with ANUG who are not allergic to penicillin.
500 mg PO qid for 10 d
<12 years: 25-50 mg/kg/d PO divided q6-8h; not to exceed 3 g/d (250 mg = 400,000 U)
>12 years: Administer as in adults
Probenecid may increase effectiveness by decreasing clearance; tetracyclines are bacteriostatic, causing a decrease in the effectiveness of penicillins when administered concurrently
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in renal impairment
Alternative DOC for patients allergic to penicillin.
1-2 h before the procedure: 1 g PO
6 h after initial dose: 500 mg PO
250 mg erythromycin stearate/base (or 400 mg ethylsuccinate) q6h 1 h ac, or 500 mg q12h
Alternatively, 333 mg q8h; increase, depending on infection severity, up to 4 g/d
2 h prior to procedure: 20 mg/kg PO
6 h after initial dose: 10 mg/kg PO
Age, weight, and severity of infection determine proper dosage
30-50 mg/kg/d (15-25 mg/lb/d) in divided doses; double the dose for severe infection
Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis
Documented hypersensitivity; hepatic impairment
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in liver disease; estolate formulation may cause cholestatic jaundice; adverse GI effects are common (give doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occur
Used as an adjunct to scaling and root planing procedures for reduction of pocket depth in patients with adult periodontitis. May be used as part of a periodontal maintenance program that includes good oral hygiene and scaling and root planing.
Insert a unit-dose cartridge into base of pocket and then press the thumb ring in the handle mechanism to expel the powder while gradually withdrawing the tip from the base of the pocket; the handle mechanism should be sterilized between patients; minocycline microspheres do not have to be removed, as they are bioresorbable, and no adhesive or dressing is required
Not established
None reported
Documented hypersensitivity
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Discoloration of teeth may occur in last half of pregnancy, infancy, and childhood to age 8 y (do not use unless benefits outweigh risks); photosensitivity may occur; use of minocycline microspheres in acutely abscessed periodontal pocket has not been studied and is not recommended; use of minocycline microspheres may result in overgrowth of nonsusceptible microorganisms, including fungi; effect of treatment for > 6 mo has not been studied; use minocycline microspheres with caution in patients with history of predisposition to oral candidiasis; safety and efficacy of minocycline microspheres has not been established for treatment of periodontitis in patients with coexistent oral candidiasis; use of microspheres has not been clinically tested in patients with immunocompromise (eg, diabetes, chemotherapy, radiation therapy, HIV infection)
Inhibits protein synthesis and thus bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria. However, some studies have shown that doxycycline reduces elevated collagenase activity in gingival crevicular fluid of patients with adult periodontitis. Clinical significance of these findings is not known.
Following scaling and root planing: 20 mg PO bid as an adjunct for <9 mo; safety beyond 12 mo and efficacy beyond 9 mo have not been established
Not established
Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; tetracyclines can increase hypoprothrombinemic effects of anticoagulants; tetracyclines can decrease effects of oral contraceptives, causing breakthrough bleeding and increased risk of pregnancy
Documented hypersensitivity; severe hepatic dysfunction
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last one half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines
Alternative for penicillin-allergic patients, a popular choice for severe infections or those recalcitrant with penicillin.
300 mg PO tid
6-8 mg/kg/d PO divided tid/qid
Increases duration of neuromuscular blockade, induced by tubocurarine and pancuronium; erythromycin may antagonize effects of clindamycin; antidiarrheals may delay absorption of clindamycin
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis
This is shown to decrease bacterial counts in oral flora. It probably speeds resolution of gingivitis when combined with brushing and flossing.
Has bactericidal activity.
15 mL (1 tablespoon); swish in mouth for 30 s and expectorate bid
Not established
None reported
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
May stain tooth enamel
Patients with ANUG should be given a strong analgesic along with topical anesthetics and NSAIDs because pain control is very important in allowing the patient to eat and carry out toothbrushing, flossing, and other oral hygiene maneuvers necessary to eradicate the disease. NSAIDs also help to decrease pain. Although effects of NSAIDs in the treatment of pain tend to be patient-specific, ibuprofen usually is the DOC for initial therapy.
Narcotic analgesic well tolerated by most patients; it may induce severe nausea and vomiting in patients particularly sensitive to the drug.
1-2 tab PO q6h prn pain
0.5-1 mg/kg/dose PO based on codeine q4-6h; 10-15 mg/kg/dose PO based on acetaminophen content; not to exceed 2.6 g/d of acetaminophen
Toxicity increases with CNS depressants or tricyclic antidepressants
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in patients dependent on opiates since this substitution may result in acute opiate-withdrawal symptoms; caution in severe renal or hepatic dysfunction
Used for pain relief and to decrease gingival inflammation. Use with care in patients with history of asthma or peptic ulcer disease.
600 mg PO q6-8h
5 mg/kg PO q6-8h
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy
These agents are helpful in providing pain control, which is very important in allowing the patient to carry out toothbrushing, flossing, and other oral hygiene maneuvers.
An adjunctive therapy for pain control that decreases the permeability to sodium ions in neuronal membranes. This results in inhibition of depolarization, blocking the transmission of nerve impulses.
15 mL rinse PO and expectorate q6-8h prn
>12 years: 15 mL rinse PO and expectorate q6-8h prn
None reported
Documented hypersensitivity; Adams-Stokes syndrome and Wolff-Parkinson-White syndrome
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
For external or mucous membrane use only; do not use in eyes
Idigbe EO, Enwonwu CO, Falkler WA, et al. Living conditions of children at risk for noma: Nigerian experience. Oral Dis. Apr 1999;5(2):156-62. [Medline].
Dorfer CE, Becher H, Ziegler CM, et al. The association of gingivitis and periodontitis with ischemic stroke. J Clin Periodontol. May 2004;31(5):396-401. [Medline].
Hujoel PP, Drangsholt M, Spiekerman C, DeRouen TA. Periodontal disease and coronary heart disease risk. JAMA. Sep 20 2000;284(11):1406-10. [Medline].
Wu T, Trevisan M, Genco RJ, et al. Periodontal disease and risk of cerebrovascular disease: the first national health and nutrition examination survey and its follow-up study. Arch Intern Med. Oct 9 2000;160(18):2749-55. [Medline].
Bobetsis YA, Barros SP, Offenbacher S. Exploring the relationship between periodontal disease and pregnancy complications. J Am Dent Assoc. Oct 2006;137 Suppl 2:7S-13S. [Medline].
Mealey BL. Periodontal disease and diabetes: A two-way street. J Am Dent Assoc. Oct 2006;137 Suppl 2:26S-31S. [Medline].
Perez A, Wagner AM, Carreras G, et al. Prevalence and phenotypic distribution of dyslipidemia in type 1 diabetes mellitus: effect of glycemic control. Arch Intern Med. Oct 9 2000;160(18):2756-62. [Medline].
Lorenz K, Bruhn G, Heumann C, et al. Effect of two new chlorhexidine mouthrinses on the development of dental plaque, gingivitis, and discolouration. A randomized, investigator-blind, placebo-controlled, 3-week experimental gingivitis study. J Clin Periodontol. Aug 2006;33(8):561-7. [Medline].
Zimmer S, Kolbe C, Kaiser G, et al. Clinical efficacy of flossing versus use of antimicrobial rinses. J Periodontol. Aug 2006;77(8):1380-5. [Medline].
Triratana T, Rustogi KN, Volpe AR, et al. Clinical effect of a new liquid dentifrice containing triclosan/copolymer on existing plaque and gingivitis. J Am Dent Assoc. Feb 2002;133(2):219-25. [Medline].
Taiyeb Ali TB, Waite IM. The effect of systemic ibuprofen on gingival inflammation in humans. J Clin Periodontol. Nov 1993;20(10):723-8. [Medline].
Johnson RH, Armitage GC, Francisco C, Page RC. Assessment of the efficacy of a nonsteroidal anti-inflammatory drug, Naprosyn, in the treatment of gingivitis. J Periodontal Res. Jul 1990;25(4):230-5. [Medline].
Cronin M, Dembling W, Warren PR, King DW. A 3-month clinical investigation comparing the safety and efficacy of a novel electric toothbrush (Braun Oral-B 3D Plaque Remover) with a manual toothbrush. Am J Dent. Sep 1998;11(Spec No):S17-21. [Medline].
Forrest JL, Miller SA. Manual versus powered toothbrushes: a summary of the Cochrane Oral Health Group's Systematic Review. Part II. J Dent Hyg. Spring 2004;78(2):349-54. [Medline].
Bahekar AA, Singh S, Saha S, Molnar J, Arora R. The prevalence and incidence of coronary heart disease is significantly increased in periodontitis: a meta-analysis. Am Heart J. Nov 2007;154(5):830-7. [Medline].
Briggs GG, Freeman RK, Yaffe SJ. Drugs in Pregnancy and Lactation. 6th ed. Lippincott Williams & Wilkins; 2001.
Estafan D, Gultz J, Kaim JM, et al. Clinical efficacy of an herbal toothpaste. J Clin Dent. 1998;9(2):31-3. [Medline].
Falkler WA Jr, Enwonwu CO, Idigbe EO. Microbiological understandings and mysteries of noma (cancrum oris). Oral Dis. Apr 1999;5(2):150-5. [Medline].
Gaspar L, Suri C, Toth BZ, et al. [Experience with clindamycin in stomatologic diseases]. Fogorv Sz. Aug 1999;92(8):251-8. [Medline].
Gehlen I, Netuschil L, Georg T, et al. The influence of a 0.2% chlorhexidine mouthrinse on plaque regrowth in orthodontic patients. A randomized prospective study. Part II: Bacteriological parameters. J Orofac Orthop. 2000;61(2):138-48. [Medline].
Greenspan JS. Oral manifestation of disease. In: Fauci, et al, eds. Harrison's Principles of Internal Medicine. 13th ed. McGraw Hill; 1994:199-200.
Guggenheimer J, Eghtesad B, Close JM, Shay C, Fung JJ. Dental health status of liver transplant candidates. Liver Transpl. Feb 2007;13(2):280-6. [Medline].
Howell RB, Jandinski JJ, Palumbo P, et al. Oral soft tissue manifestations and CD4 lymphocyte counts in HIV-infected children. Pediatr Dent. Mar-Apr 1996;18(2):117-20. [Medline].
Lamster IB, Grbic JT, Mitchell-Lewis DA, et al. New concepts regarding the pathogenesis of periodontal disease in HIV infection. Ann Periodontol. Jul 1998;3(1):62-75. [Medline].
Ranney RR. Diagnosis of periodontal diseases. Adv Dent Res. Dec 1991;5:21-36. [Medline].
Robinson PJ. Gingivitis: a prelude to periodontitis?. J Clin Dent. 1995;6 Spec No:41-5. [Medline].
Sculleya DV, Langley-Evansa SC. Salivary antioxidants and periodontal disease status. Proceedings of the Nutrition Society [serial online]. 2002;61:137-143. Accessed September 28, 2008. Available at http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=804048.
gingivitis, gum swelling, swollen gums, bleeding gums, gum disease, acute necrotizing ulcerative gingivitis, periodontal disease, ANUG, trench mouth, inflammation of the gingiva, plaque, bacterial plaque, gum swelling, gingival tissue, gingiva, acute infectious gingivitis, Prevotella intermedia, alpha-hemolytic streptococci, Actinomyces species, noma, cancrum oris, chronic gingivitis, blood dyscrasias, inadequate oral hygiene, halitosis, gingival hyperplasia, gingivostomatitis
James M Stephen, MD, FAAEM, FACEP, Assistant Professor, Tufts University School of Medicine; Attending Physician and Director of Medical Informatics, Department of Emergency Medicine, Associate Director, Kiwanis Pediatric Trauma Service, Tufts Medical Center
James M Stephen, MD, FAAEM, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians
Disclosure: Nothing to disclose.
Michael Glick, DMD, Professor and Acting Chair, Department of Diagnostic Sciences, New Jersey Dental School, University of Medicine and Dentistry of New Jersey
Michael Glick, DMD is a member of the following medical societies: American Academy of Oral Medicine and American Dental Association
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Mark W Fourre, MD, Program Director, Department of Emergency Medicine, Maine Medical Center; Associate Clinical Professor, Department of Surgery, University of Vermont School of Medicine
Disclosure: Nothing to disclose.
John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Steven C Dronen, MD, FAAEM, Director of Emergency Services, Director of Chest Pain Center, Department of Emergency Medicine, Ft Sanders Sevier Medical Center
Steven C Dronen, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.