Apical periodontitis (AP) is an inflammatory reaction of the periapical tissues of a tooth and subsequent infection of the root canal system (Kakehashi et al., 1965). Pulp necrosis can occur after the invasion of microorganisms into the tooth and is usually the result of an irreversible inflammatory response in the pulp. After pulp necrosis, the microorganisms invade the root canal system until they eventually reach the root apex (Moller et al., 1981). To confine the infection a complex inflammatory response starts in the area where the root canal meets the periapical tissues. Locally, the jaw bone is resorbed, in order to make space for inflammatory tissue.

Thus, AP is the consequence of a complex interplay between microbes, their virulence factors and the immune system of the host (Marton & Kiss 2014). The local activation of the host’s innate and adaptive immune system is characterized by the recruitment of various cell types and cell-specific mediators, which results in the destruction of tooth supporting tissues and the formation of periapical lesions (i.e. granuloma, abscess and/or cyst; Marton&  Kiss 2014).

Apical periodontitis can modify the systemic levels of inflammatory markers e.g., high-sensitivity C-reactive protein (hs-CRP), (IL-1β), IL-6, IL-12, IL-10, tumour necrosis factor (TNF-α), matrix metalloproteinases (MMP-8 and MMP-9), soluble vascular cell adhesion molecule 1 (sVCAM-1), endothelial leukocyte adhesion molecule (E-selectin) and intercellular adhesion molecule (ICAM)), Immunoglobulin (Ig) A, IgM, IgG, asymmetric dimethylarginine (ADMA) and complement-C3 levels) in humans . This can contribute to increased systemic inflammation.

The study is thus planned to evaluate inflammatory marker levels in patients with apical periodontitis using Photodynamic therapy. PDT in Endodontics has been tested in termed of bacterial load reduction in vivo, in vitro, ex vivo. It uses visible light source of a 632 nm (630-700nm) wavelength, generally a low intensity diode or light-emitting diode (LED) is absorbed by a non-toxic photosensitizer (PS) produces antimicrobial effect leading to bacterial load reduction.

AIMS AND OBJECTIVES

1.     Evaluation of inflammatory biomarkers level (IL-6) in serum of patient with apical periodontitis.

2.     To find the effect of PDT on systemic inflammatory biomarkers (IL-6) using patient serum.

3. CBCT evaluation of size of periapical lesion pre and post procedure.

MATERIALS AND METHODS:

            The present study will be conducted in the department of Conservative Dentistry and Endodontics, Faculty of Dental Sciences, King George’s Medical University, Lucknow

            Patients of age group 18 to 40 years with radiographic evidence of periapical lesion(s)  will be selected for study. The presence and scoring of periapical lesion will be measured using CBCT and graded according to the  Periapical Index by Dag Orstavik. The Effect of PDT and systemic markers will be evaluated using patient serum.

Radiographic examination: The presence of the lesion will be confimed using Cone beam computed tomography (CBCT) imaging. The severity of the disease will be graded using the Periapical Index (CBCT-PAI). All findings will be recorded.

Measurement of Level of inflammatory biomarkers: 10 ml of patient’s blood will be withdrawn and level of IL-6 will be measured in the serum. All laboratory procedures will be carried in the Department of Microbiology using standard testing kits and protocols.

All patients recruited in the study ( cases and controls ) will be given endodontic therapy for the teeth affected with the endodontic disease.

            Data obtained will be statistically analysed.