At the forefront of dentistry today is an increasing knowledge of the role of chronic inflammation and the changes it can cause in both the oral cavity and systemically. Now you can gain a new level of understanding with these informative articles to help you more effectively treat your patients with gingival inflammation. Originally appearing in the July 2004 Supplement to the Compendium of Continuing Education in Dentistry entitled, "Gingivitis: An Inflammatory Periodontal Disease" these articles are available to you online at www.ColgateProfessional.com or by calling your Colgate Representative.
Inflammation is the localized, protective response of the body to injury or infection. The classic clinical signs that characterize inflammation are heat, redness, swelling, pain, and loss of function. During inflammation, cells and their secreted chemicals attempt to destroy, dilute, or wall off the injurious agent. A series of biochemical events cause the blood vessels to dilate and become more permeable, resulting in the activation of the complement, clotting and kinin systems. The end result of inflammation is the return of function by the regeneration or repair of the affected tissue. In some instances, inflammation may continue for a prolonged period of time, producing untoward consequences for localized tissue as well as the entire body.The purpose of this article is to provide a basic and simplified understanding of how the inflammatory process functions in the human body.
Frank A. Scannapieco, DMD, PhD
There has been a resurgence of interest in recent years in the systemic effects of oral infections such as periodontal diseases. The study of the various means by which periodontal infections and inflammation may influence a variety of systemic conditions is collectively referred to as periodontal medicine. The periodontium responds to toothborne biofilm (dental plaque) by the process of inflammation. Dental biofilms release a variety of biologically active products, such as bacterial lipopolysaccharides (endotoxins), chemotactic peptides, protein toxins, and organic acids. These molecules stimulate the host to produce a variety of responses, among them the production and release of potent agents known as cytokines. These include interleukin-1 beta, interleukin-8, prostaglandins, and tumor necrosis factor-alpha. There is a spectrum of periodontal response to these molecules, from mild gingivitis to severe destructive periodontitis. These and other host products and responses may influence a variety of important disease pathways, including atherosclerosis, mucosal inflammation, and premature parturition. The purpose of this article is to review the possible biological pathways by which periodontal diseases may influence these disease processes.