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Gingival inflammation treatment options

8th November 2011 0
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According to the Spanish Society of Periodontology and Osseointegration, gingivitis and periodontitis are the two most common diseases among human beings, affecting 59.8% of all adults between ages 35 and 44 and 51.6% of all patients between ages 65 and 74. More than half of the Spanish adult population has gingivitis. 

Gerardo Gómez-Moreno1, Antonio Aguilar-Salvatierra2, Javier Guardia3 y José Luis Calvo-Guirado4 
In the 90s, dental plaque became accepted as a biofilm, which is composed of bacteria that represent 15-20% of plaque volume, embedded in a matrix or glycocalyx, which constitutes the remaining 75-80%1. This matrix is a combination of exopolysaccharides, proteins, mineral salts and cell material2. The oral biofilm is the main etiological agent of caries and gum disease (gingivitis and periodontitis)3. A qualitative and quantitative alteration in this bacterial population is the key for maintaining oral health4
Gingivitis is defined as the inflammation of gums caused by biofilm deposits that ultimately irritate and inflame them. Bacteria and their toxins cause infection and inflammation in the gums, causing gingival sensitivity5. Gingivitis affects soft gingival tissues and is reversible. If gingivitis is not kept under control, it can evolve into periodontitis, extending to the deepest areas, such as the periodontal ligament and the alveolar bone6

Factors involved: 

Many factors exist that can favour the manifestation of gingivitis7
Gingivitis associated with local factors: can develop both in healthy and in reduced, but stable, periodontia5, generally associated with local retention factors of the biofilm, such as deficient oral hygiene, tooth malposition, occlusal trauma, overextended restorations, fixed and removable orthodontic appliances and prostheses (bridges and crowns), the latter two possibly irritating the gums and therefore increasing the risk for gingivitis. 
Gingivitis associated with systemic factors: is characterized by being modified in its evolutionary course by diverse general effects such as5 
- The endocrine system, among which we find gingivitis associated with pregnancy, puberty, menstrual cycle and uncontrolled diabetes.
- Blood dyscrasia, such as thrombocytopenia purpura, due to abnormal functioning or number of blood cells. 
 

Bibliography

  1. Serrano-Granger J, Herrera D. “La placa dental como biofilm. ¿Cómo eliminarla?”. RCOE. 2005;10(4):431-9. 
  2. Donlan RM, Costerton JW. “Biofilms: survival mechanisms of clinically relevant microorganisms”. Clin Microbiol Rev. 2002 Apr;15(2):167-93. 
  3. Enrile de Rojas FJ, Santos-Alemany A. “Colutorios para el control de placa y gingivitis basados en la evidencia científica”.RCOE. 2005;10(4):445-52. 
  4. Costerton JW. Biofilms: “Survival Mechanisms of Clinically Relevant Microorganisms”. Clinical Microbiology Reviews 2002;167-93. 
  5. American Academy of Periodontology. “Parameter on plaqueinduced gingivitis”. J Periodontol. 2000;7:851-852. 
  6. Becerik S, Türkoğlu O, Emingil G, Vural C, Ozdemir G, Atilla G. “Antimicrobial effect of adjunctive use of chlorhexidine mouthrinse in untreated gingivitis: a randomized, placebo-controlled study”. APMIS. 2011 Jun;119(6):364-72. 
  7. Matesanz-Pérez P, Matos-Cruz R, Bascones-Martínez A. “Enfermedades gingivales: una revisión de la literatura”. Av Periodon Implantol. 2008;20(1): 11-25. 
  8. Bascones-Martinez A, Matesanz-Perez P, Escribano-Bermejo M, González-Moles MA, Bascones-Ilundain J, Meurman JH.“Periodontal disease and diabetes-Review of the Literature”. Med Oral Patol Oral Cir Bucal. 2011. En prensa. 
  9. Ridker PM. “Fibrinolytic and inflammatory markers for arterial occlusion: the evolving epidemiology of thrombosis and hemostasis”. Thromb Haemost 1997; 78:53-9. 
  10. Drangsholt MT. “A new casual model of dental diseases associated with endocarditis”. Ann Periodontol 1998; 3:184. 
  11. Hayes C, Sparrow D, Cohen M, Vokonas PS, Garcia RI. “The association between alveolar bone loss and pulmonary function: the VA Dental Longitudinal Study”. Ann Periodontol 1998;3:257-61. 
  12. Jansen J, Liljemark W, Bloomquist C. “The effect of female sex hormones on subgingival plaque”. J Periodontol 1981;52: 599-602. 
  13. Offenbacher S, Katz V, Fertik G, Collins J, Boyd D, Maynor G, et al. “Periodontal infection as a possible risk factor for preterm low birth weight”. J Periodontol 1996;67:103–13. 
  14. Herrera D, Roldán S, Santacruz I, Santos S, Masdevall M, Sanz M. “Differences in antimicrobial activity of four commercial 0.12% chlorhexidine mouthrinse formulations: an in vitro contact test and salivary bacterial counts study”. J Clin Periodontol. 2003 Apr;30(4):307-14. 
  15. Gunsolley, J. C. (2006) “A meta‐analysis of six‐month studies of antiplaque and antigingivitis agents”. J Am Dent Assoc 137, 1649‐1657. 
  16. Pitten, F. A. & Kramer, A. (2001) “Efficacy of cetylpyridinium chloride used as oropharyngeal antiseptic”. Arzneimittelforschung 51, 588‐595. 
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