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It is well known that biofilm and calculus responsible for periodontal disease can be of different nature depending on their supra or subgingival location, and that the physical or chemical methods used for their elimination, achieve different results in both places (Davies et al., 1998). Since the use of laser confocal microscope and the study of biofilms in their natural state, it has been observed that the behaviour of bacteria is quite different to the observed in traditional cultures. In their natural state, the bacterial colonies are constituted by several microcolonies included in a matrix, which has canals through which flow fluids transporting nutrients, metabolic wastes, enzymes, oxygen and other products enabling the presence of different environments (Costerton et al. 1987). The biofilms adhered on the internal and external walls of the periodontal pocket, the free biofilm and the possibility of a bacterial penetration through the epithelium to the underlying connective tissue can cause a gingival inflammatory reaction. This inflammation may progress with vasodilation, cellular migration and release of mediators, thus increasing the inflammatory response and perpetuating the disease. This situation makes microorganisms more resistant to drugs, which frequently are unable to reach the colonies protected by the matrix and by the presence of resistent bacteria (Donlan & Costerton, 2002). The inflammatory phenomena triggered by the bacteria and their waste products attracts macrophages that produce, among others, interleukin 1 (IL-1) and tumor necrosis factor alfa (TNF-┙), which have the ability to activate osteoclasts and produce bone resorption. TNF-┙ activates the adhesion molecules of the endothelial cells of the vessels, favouring the adhesion of monocytes and diapedesis. It also stimulates the arrival of T lymphocytes, which contribute with receptor activator of nuclear factor kappa B ligand (RANKL) to the bone, consequently favouring the bone loss (Kong et al., 1999). But this process is more complex as it needs some proteins such as nuclear factor kappa B (NF-kB), receptor activator of nuclear factor kappa B (RANK), RANKL and osteoprotegerin (OPG), among others, which may change the answer of the osteoclast precursors and therefore modify the osseous destruction. The NF-kB plays a basic role as activator of immunoglobulins during the infectious process (Gilmore, 2006). So, as IL-1 and TNF-┙ favour the synthesis of RANK-L

Laser Radiation as an Adjunct to Nonsurgical Treatment of Periodontal Disease