Gingivitis

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Gingivitis
Classification and external resources
Gingivitis-before-and-after-3.jpg
Gingivitis before (top) and after (bottom) a thorough mechanical debridement of the teeth.
ICD-10 K05.0-K05.1
ICD-9 523.0-523.1
DiseasesDB 34517
MedlinePlus 001056
MeSH D005891

Gingivitis ("inflammation of the gum tissue") is a non-destructive periodontal disease.[1] The most common form of gingivitis, and the most common form of periodontal disease overall, is in response to bacterial biofilms (also called plaque) adherent to tooth surfaces, termed plaque-induced gingivitis. In the absence of treatment, gingivitis may progress to periodontitis, which is a destructive form of periodontal disease. The most common form of gingivitis and periodontal disease occurs in response to bacterial biofilms (also called plaque) adherent to tooth surfaces, and is thus termed plaque-induced gingivitis. Gingivitis is reversible with good oral hygiene. However in the absence of treatment, or if not controlled, gingivitis can progress to periodontitis- where the inflammation results in tissue destruction and alveolar bone resorption, which can ultimately lead to tooth loss[2]

While in some sites or individuals gingivitis never progresses to periodontitis,[3] data indicates that periodontitis is always preceded by gingivitis.[4]

Classification[edit]

As defined by the 1999 World Workshop in Clinical Periodontics, there are two primary categories of gingival diseases, each with numerous subgroups:[5]

  1. Dental plaque-induced gingival diseases.
    1. Gingivitis associated with plaque only
    2. Gingival diseases modified by systemic factors
    3. Gingival diseases modified by medications
    4. Gingival diseases modified by malnutrition
  2. Non-plaque-induced gingival lesions
    1. Gingival diseases of specific bacterial origin
    2. Gingival diseases of viral origin
    3. Gingival diseases of fungal origin
    4. Gingival diseases of genetic origin
    5. Gingival manifestations of systemic conditions
    6. Traumatic lesions
    7. Foreign body reactions
    8. Not otherwise specified

Signs and symptoms[edit]

The symptoms of gingivitis are somewhat non-specific and manifest in the gum tissue as the classic signs of inflammation:

  • Swollen gums
  • Bright red or purple gums
  • Gums that are tender or painful to the touch
  • Bleeding gums or bleeding after brushing and/or flossing
  • Bad breath (halitosis)

Additionally, the stippling that normally exists on the gum tissue of some individuals will often disappear and the gums may appear shiny when the gum tissue becomes swollen and stretched over the inflamed underlying connective tissue. The accumulation may also emit an unpleasant odor. When the gingiva are swollen, the epithelial lining of the gingival crevice becomes ulcerated and the gums will bleed more easily with even gentle brushing, and especially when flossing.

Risk factors[edit]

Risk factors associated with gingivitis are:

  • increase in age
  • low socio-economic status
  • poor education
  • low dental care utilization
  • poor oral hygiene levels
  • smoking
  • psychosocial stress and genetic factors
  • pre-existing conditions

Cause[edit]

Because plaque-induced gingivitis is by far the most common form of gingival diseases, the following sections will deal primarily with this condition.

The etiology, or cause, of plaque-induced gingivitis is bacterial plaque, which acts to initiate the body's host response. This, in turn, can lead to destruction of the gingival tissues, which may progress to destruction of the periodontal attachment apparatus.[6] The plaque accumulates in the small gaps between teeth, in the gingival grooves and in areas known as plaque traps: locations that serve to accumulate and maintain plaque. Examples of plaque traps include bulky and overhanging restorative margins, claps of removable partial dentures and calculus (tartar) that forms on teeth. Although these accumulations may be tiny, the bacteria in them produce chemicals, such as degrative enzymes, and toxins, such as lipopolysaccharide (LPS, otherwise known as endotoxin) or lipoteichoic acid (LTA), that promote an inflammatory response in the gum tissue. This inflammation can cause an enlargement of the gingiva and subsequent formation. Early plaque in health consists of a relatively simple bacterial community dominated by Gram-positive cocci and rods. As plaque matures, and gingivitis develops, the communities become increasingly complex with higher proportions of Gram-negative rods, fusiforms, filaments, spirilla and spirochetes. Later experimental gingivitis studies, using culture, provided more information regarding the specific bacterial species present in plaque. Taxa associated with gingivitis included Fusobacterium nucleatum subsp. polymorphum, Lachnospiraceae [G-2] sp. HOT100, Lautropia sp. HOTA94, and Prevotella oulorum, whilst Rothia dentocariosa was associated with periodontal health. Further study of these taxa is warranted and may lead to new therapeutic approaches to prevent periodontal disease.

Diagnosis[edit]

Gingivitis is a category of periodontal disease where there is no loss of bone but there is presence of inflammation and bleeding.

Each tooth is divided into four gingival units (mesial, distal, buccal, and lingual) and given a score from 0-3 based on the gingival index. The four scores are then averaged to give each tooth a single score. Gingivitis is a category of periodontal disease where there is no loss of bone but there is presence of inflammation and bleeding.

The diagnosis of the periodontal disease Gingivitis is done by a dentist. The diagnosis is based on clinical assessment data acquired during a comprehensive periodontal exam. Either a registered dental hygienist or a dentist may perform the comprehensive periodontal exam but the data interpretation and diagnosis is done by the dentist. The comprehensive periodontal exam consists of a visual exam, a series of radiographs, probing of the gingiva, determine the extent of current or past damage to the periodontium and a comprehensive review of the medical and dental histories.

Current research shows that activity levels of the following enzymes in saliva samples are associated with periodontal destruction: asparatate aminotransferase (AST), alanine aminotransferase (ALT), gamma glutamyl transferase (GGT), alkaline phosphatase (ALP), and acid phosphatase (ACP). Therefore these enzyme biomarkers may be used to aid in the diagnosis and treatment of gingivitis and periodontitis.

A dental hygienist or dentist will check for the symptoms of gingivitis, and may also examine the amount of plaque in the oral cavity. A dental hygienist or dentist will also look for signs of periodontitis using X-rays or periodontal probing as well as other methods.

If gingivitis is not responsive to treatment, referral to a periodontist (a specialist in diseases of the gingiva and bone around teeth and dental implants) for further treatment may be necessary.

Prevention[edit]

Gingivitis can be prevented through regular oral hygiene that includes daily brushing and flossing.[7] Hydrogen peroxide, saline, alcohol or chlorhexidine mouth washes may also be employed. In a recent clinical study, the beneficial effect of hydrogen peroxide on gingivitis has been highlighted.[8] Rigorous plaque control programs along with periodontal scaling and curettage also have proved to be helpful, although according to the American Dental Association, periodontal scaling and root planing are considered as a treatment to periodontal disease, not as a preventive treatment for periodontal disease.[9] In a 1997 review of effectiveness data the U.S. Food and Drug Administration (FDA) found clear evidence which showed that toothpaste containing triclosan was effective in preventing gingivitis.[10]

In many countries, such as the United States, mouthwashes containing chlorhexidine are available only by prescription.

Researchers analyzed government data on calcium consumption and periodontal disease indicators in nearly 13,000 U.S. adults. They found that men and women who had calcium intakes of fewer than 500 milligrams, or about half the recommended dietary allowance, were almost twice as likely to have gum disease, as measured by the loss of attachment of the gums from the teeth. The association was particularly evident for people in their 20s and 30s.[11]

Preventing gum disease may also benefit a healthy heart. According to physicians with The Institute for Good Medicine at the Pennsylvania Medical Society, good oral health can reduce risk of cardiac events. Poor oral health can lead to infections that can travel within the bloodstream.[12]

Treatment[edit]

Analgesic and antiseptic gum paint with applicator buds used in treatment of gingivitis

The focus of treatment for gingivitis is removal of the etiologic (causative) agent, plaque. Therapy is aimed at the reduction of oral bacteria, and may take the form of regular periodic visits to a dental professional together with adequate oral hygiene home care. Thus, several of the methods used in the prevention of gingivitis can also be used for the treatment of manifest gingivitis, such as scaling, root planing, curettage, mouth washes containing chlorhexidine or hydrogen peroxide, and flossing. Interdental brushes also help remove any causative agents.[13] At home oral hygiene therapy to eliminate gingivitis must be aimed at increasing patient motivation and teaching patients the proper techniques to remove bacteria from their teeth and gingiva. Patients are taught how to brush properly and are advised to brush twice daily for two minutes with a toothpaste that contains fluoride. They are also taught how to floss properly and advised to floss at least once daily. Oral hygiene aids must be chosen for each patient to target their specific needs and abilities.

A patient’s oral hygiene care at home must be combined with regular periodontal therapy at the dental office to remove calculus (tartar). Supragingival and subgingival calculus can be present. Calculus is removed by a dentist or dental hygienist using hand, sonic or ultrasonic instruments. The periodontal tissues must be evaluated at subsequent dental appointments to keep the diagnosis current. Both in-office treatment and home care must be modified as necessary based on the re-evaluation.

The active ingredients approved by the American Dental Association that “reduce plaque and demonstrate effective reduction of gingival inflammation over a period of time” are triclosan, chlorhexidine digluconate, and a combination of thymol, menthol, eucalyptol and methyl salicylate. These ingredients are found in toothpaste and mouthwash. These products are recommended to patiens based upon their needs.

Hydrogen Peroxide was long considered to use as over the counter agent to treat gingivitis. There has been evidence to show the positive effect on controlling gingivitis in short-term period use. Study indicates the fluoridated hydrogen peroxide-based mouth rinse can remove teeth stain and reduce gingivitis

Recent scientific studies have also shown the beneficial effects of mouthwashes with essential oils.[14]

Furthermore, oral Non-Steroidal Anti-Inflammatory Drug (NSAID) rinses are a relatively new treatment modality for treating inflammation in the oral cavity. NSAIDs such as ibuprofen or diclofenac, are a mainstay of analgesic and anti-inflammatory treatment in dentistry. However, the systemic use of NSAID's are associated with ulcerogenic effects and several other side-effects, namely gastric irritability, fluid-retention and nephrotoxicity; among these gastric irritability is most common. Therefore, it is preferable to use local formulations such as mouthwashes to treat oral inflammatory conditions e.g. gingivitis. A randomized, investigator-blind, clinical study published in September, 2011, showed the new Diclofenac Epolamine (diclofenac N-(2-hydroxyethyl) Pyrrolidine; DHEP), a diclofenac salt with greater water solubility, as an effective and tolerable medicinal product for symptomatic and post-surgical relief of inflammation of the oral cavity.[15] Volunteers with inflammatory conditions, of which gingivitis was most prevalent, treated with DHEP, experienced a significantly greater reduction in pain and inflammation and were also free of pain and inflammatory symptoms as soon as Day 3 of the study compared to those treated with merely 0.0075% diclofenac mouthwash.[15] There was an even greater reduction relative to the placebo group.[16]

Moreover, studies published in the Journal of Periodontology comparing the NSAID’s, Celcoxib or Etorcoxib and the corticosteroid, dexamethasone also showed the power and efficacy of using proper NSAID therapy to combat oral inflammation.[17] The results of these studies showed the use of celecoxib or dexamethasone as effective for the prevention and preemptive control of postoperative pain after periodontal surgery.[13] Another affective treatment option for people with gingivitis is full mouth ultrasonic debridement. It helps with plaque/bleeding on probing, pocket depth, relative recession, and relative probing attachment level at baseline. The level of effectiveness varies from smokers and non-smokers, however. Smokers experienced less effective results overall, despite using a non-surgical technique.

Overall, Intensive oral hygiene care has been shown to dramatically improves gingival health in individuals with well-controlled type 2 diabetes. Periodontal destruction is also slowed down due to the extensive oral care. Intensive oral hygiene care (oral health education plus supra-gingival scaling) without any periodontal therapy improves gingival health, and may prevent progression of gingivitis in well-controlled diabetes.

Complications[edit]

See also[edit]

References[edit]

  1. ^ The American Academy of Periodontology. Proceedings of the World Workshop in Clinical Periodontics. Chicago:The American Academy of Periodontology; 1989:I/23-I/24.
  2. ^ "Parameter on Plaque-Induced Gingivitis". Journal of Periodontology 71 (5 Suppl): 851–2. 2000. doi:10.1902/jop.2000.71.5-S.851. PMID 10875689. 
  3. ^ Ammons, WF; Schectman, LR; Page, RC (1972). "Host tissue response in chronic periodontal disease. 1. The normal periodontium and clinical manifestations of dental and periodontal disease in the marmoset". Journal of periodontal research 7 (2): 131–43. doi:10.1111/j.1600-0765.1972.tb00638.x. PMID 4272039. 
  4. ^ Page, RC; Schroeder, HE (1976). "Pathogenesis of inflammatory periodontal disease. A summary of current work". Laboratory investigation; a journal of technical methods and pathology 34 (3): 235–49. PMID 765622. 
  5. ^ Armitage, Gary C. (1999). "Development of a Classification System for Periodontal Diseases and Conditions". Annals of Periodontology 4 (1): 1–6. doi:10.1902/annals.1999.4.1.1. PMID 10863370. 
  6. ^ Research, Science and Therapy Committee of the American Academy of Periodontology (2001). "Treatment of Plaque-Induced Gingivitis, Chronic Periodontitis, and Other Clinical Conditions". Journal of Periodontology 72 (12): 1790–1800. doi:10.1902/jop.2001.72.12.1790. PMID 11811516. 
  7. ^ Sambunjak, D.; Nickerson, J. W.; Poklepovic, T.; Johnson, T. M.; Imai, P.; Tugwell, P.; Worthington, H. V. (2011). "Flossing for the management of periodontal diseases and dental caries in adults". In Johnson, Trevor M. Cochrane Database of Systematic Reviews. doi:10.1002/14651858.CD008829.pub2.  edit
  8. ^ Hasturk, Hatice; Nunn, Martha; Warbington, Martha; Van Dyke, Thomas E. (2004). "Efficacy of a Fluoridated Hydrogen Peroxide-Based Mouthrinse for the Treatment of Gingivitis: A Randomized Clinical Trial". Journal of Periodontology 75 (1): 57–65. doi:10.1902/jop.2004.75.1.57. PMID 15025217. 
  9. ^ American Dental Hygienists’ Association Position Paper on the Oral Prophylaxis, Approved by the ADHA Board of Trustees April 29, 1998
  10. ^ FDA Triclosan: What Consumers Should Know Accessed 2010-08-12
  11. ^ Calcium Reduces Risk for Gum Disease. Perio.org. Retrieved on 2011-04-30.
  12. ^ Good Oral Health Can Help Your Heart, Institute for Good Medicine at the Pennsylvania Medical Society, 2009.
  13. ^ a b Steffens, J. P.; Santos, F. B. A.; Sartori, R.; Pilatti, G. L. (2010). "Preemptive Dexamethasone and Etoricoxib for Pain and Discomfort Prevention After Periodontal Surgery: A Double-Masked, Crossover, Controlled Clinical Trial". Journal of Periodontology 81 (8): 1153–1160. doi:10.1902/jop.2010.100059. PMID 20367520.  edit
  14. ^ Stoeken, Judith E.; Paraskevas, Spiros; Van Der Weijden, Godefridus A. (2007). "The Long-Term Effect of a Mouthrinse Containing Essential Oils on Dental Plaque and Gingivitis: A Systematic Review". Journal of Periodontology 78 (7): 1218–28. doi:10.1902/jop.2007.060269. PMID 17608576. 
  15. ^ a b http://www.ingentaconnect.com/content/adis/cdi/2012/00000032/00000001/art00004
  16. ^ http://www.ncbi.nlm.nih.gov/pubmed/20930354
  17. ^ Pilatti, G. L.; André Dos Santos, F. B.; Bianchi, A.; Cavassim, R.; Tozetto, C. I. W. (2006). "The Use of Celecoxib and Dexamethasone for the Prevention and Control of Postoperative Pain After Periodontal Surgery". Journal of Periodontology 77 (11): 1809–1814. doi:10.1902/jop.2006.060128. PMID 17076604.  edit

External links[edit]