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Gingivitis Information

Gingivitis ("inflammation of the gum tissue") is a term used to describe non-destructive periodontal disease.[1] The most common form of gingivitis is in response to bacterial biofilms (also called plaque) adherent to tooth surfaces, termed plaque-induced gingivitis, and is the most common form of periodontal disease. In the absence of treatment, gingivitis may progress to periodontitis, which is a destructive form of periodontal disease.[2]

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

Contents

Classification

As defined by the 1999 World Workshop in Clinical Periodontics, there are two primary categories of gingival diseases, each with numerous subgroups. Both Subgroups are extremely contagious:[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

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

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.

Cause

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.

Diagnosis

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

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

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.

Recent scientific studies have also shown the beneficial effects of mouthwashes with essential oils.[13]

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 several side-effects, namely cardiovascular thrombotic events, such as myocardial infarction and stroke, gastric irritability or ulcerogenic effects, blood dyscrasias, and nephrotoxicity; among these gastric irritability is most common. Therefore, it is preferable to use local formulations such as a mouthwash 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.[14] 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.[18]

Complications

See also

Dentistry portal

References

  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. 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. http://perio.org/resources-products/classification.pdf.
  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.
  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. ^ 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.
  14. ^ http://www.ingentaconnect.com/content/adis/cdi/2012/00000032/00000001/art00004
  15. ^ 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.
  18. ^ 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.

External links

Periodontology
Tissues of the periodontium and their physiologic entities
Diagnoses
Pathogenesis
Pathologic entities
Diagnosis, treatment planning, prevention and chemotherapeutic agents
Periodontal armamentarium
Conventional therapy
Surgical therapy and periodontal surgery
Important personalities
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Oral pathology: Stomatognathic disease (K06, K11–K14, 523, 527–529)
Vestibule of mouth
Lip Cheilitis (Angular, Actinic) · Herpes labialis · Plasma cell cheilitis · Cheilitis granulomatosa · Chapped lips Cheilitis exfoliativa · Cheilitis glandularis · Allergic contact cheilitis Drug-induced ulcer of the lip · Epidermization of the lip
Cheek Morsicatio buccarum
Oral cavity proper
Hard, soft, and periapical tissues gingival disease: Gingivitis (Desquamative gingivitis), Pericoronitis, Necrotizing ulcerative gingivitis, Noma, Epulis · Acute necrotizing ulcerative gingivitis Periodontitis · Ulcer
Salivary glands Sialadenitis (Parotitis) · Benign lymphoepithelial lesion · Necrotizing sialometaplasia · Ranula · Sialolithiasis · Mucocele of salivary gland saliva: Drooling/sialorrhea · Xerostomia
Tongue Glossitis (Geographic tongue) · Fissured tongue · Glossodynia · Black hairy tongue · Strawberry tongue · Caviar tongue · Median rhomboid glossitis · Osseous choristoma of the tongue · Smooth tongue
General Stomatitis: Aphthous ulcer (Major aphthous ulcer) · Herpetic stomatitis Velopharyngeal inadequacy oral mucosa: Erythroplakia · Leukoplakia (Hairy leukoplakia) · White sponge nevus
To be grouped from derm Acquired dyskeratotic leukoplakia · Angina bullosa haemorrhagica · Behçet syndrome · Cutaneous sinus of dental origin · Cyclic neutropenia · Epulis fissuratum · Eruptive lingual papillitis · Melanocytic oral lesion · Melkersson–Rosenthal syndrome · Mucosal lichen planus · Oral Crohn's disease · Oral florid papillomatosis · Oral melanosis · Plasmoacanthoma · Proliferative verrucous leukoplakia · Pyogenic granuloma · Pyostomatitis vegetans · Recurrent intraoral herpes simplex infection · Stomatitis nicotina · Trumpeter's wart · Vestibular papillomatosis

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Inflammation
Acute
Plasma derived mediators Bradykinin · complement (C3, C5a, MAC) · coagulation (Factor XII, Plasmin, Thrombin)
Cell derived mediators preformed: Lysosome granules · vasoactive amines (Histamine, Serotonin) synthesized on demand: cytokines (IFN-γ, IL-8, TNF-α, IL-1) · eicosanoids (Leukotriene B4, Prostaglandins) · Nitric oxide · Kinins
Chronic Macrophage · Epithelioid cell · Giant cell · Granuloma
Processes Traditional: Rubor · Calor · Tumor · Dolor (pain) · Functio laesa Modern: Acute-phase reaction/Fever · Vasodilation · Increased vascular permeability · Exudate · Leukocyte extravasation · Chemotaxis
Specific locations
Nervous CNS (Encephalitis, Myelitis) · Meningitis (Arachnoiditis) · PNS (Neuritis) · eye (Dacryoadenitis, Scleritis, Keratitis, Choroiditis, Retinitis, Chorioretinitis, Blepharitis, Conjunctivitis, Iritis, Uveitis) · ear (Otitis, Labyrinthitis, Mastoiditis)
Cardiovascular Carditis (Endocarditis, Myocarditis, Pericarditis) · Vasculitis (Arteritis, Phlebitis, Capillaritis)
Respiratory upper (Sinusitis, Rhinitis, Pharyngitis, Laryngitis) · lower (Tracheitis, Bronchitis, Bronchiolitis, Pneumonitis, Pleuritis) · Mediastinitis
Digestive mouth (Stomatitis, Gingivitis, Gingivostomatitis, Glossitis, Tonsillitis, Sialadenitis/Parotitis, Cheilitis, Pulpitis, Gnathitis) · tract (Esophagitis, Gastritis, Gastroenteritis, Enteritis, Colitis, Enterocolitis, Duodenitis, Ileitis, Caecitis, Appendicitis, Proctitis) · accessory (Hepatitis, Cholangitis, Cholecystitis, Pancreatitis) · Peritonitis
Integumentary Dermatitis (Folliculitis) · Cellulitis · Hidradenitis
Musculoskeletal

Arthritis · Dermatomyositis · soft tissue (Myositis, Synovitis/Tenosynovitis, Bursitis, Enthesitis, Fasciitis, Capsulitis, Epicondylitis, Tendinitis, Panniculitis)

Osteochondritis: Osteitis (Spondylitis, Periostitis) · Chondritis
Urinary Nephritis (Glomerulonephritis, Pyelonephritis) · Ureteritis · Cystitis · Urethritis
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female: Oophoritis · Salpingitis · Endometritis · Parametritis · Cervicitis · Vaginitis · Vulvitis · Mastitis

male: Orchitis · Epididymitis · Prostatitis · Balanitis · Balanoposthitis

pregnancy/newborn: Chorioamnionitis · Omphalitis
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