Localization of Oncostatin-M Expression in Apical Periodontitis Lesions using Immunohistochemical Analysis

The purpose of the study is to investigate the expression of Oncostatin M (OSM) in apical periodontitis lesions and to compare the expression of OSM in lesions of size greater than 5mm and lesions of size less than 5mm. OSM is a pleiotropic cytokine which has a role in the pathogenesis of many inflammatory diseases and brings about bone resorption. In our study, 30 periapical lesions of pulpal origin were collected with informed consent from the patient at the time of apical surgery. Exclusion criteria included the patients with inflammatory bone diseases like rheumatoid arthritis, osteoarthritis and patients with chronic periodontitis. All the patients are without systemic diseases and with radiographic evidence of periapical lesions including periapical alveolar bone loss. Initially non surgical endodontic treatment was attempted in these patients but the treatment has failed. Age of the patient is an important inclusion criteria in this study. Age group was standardized in the range between 20-40yrs, because in this period patients are less susceptible to systemic diseases. Paralleling cone radiographic technique was followed to get the accurate mesio-distal dimension of the lesion. The collected periapical lesions were divided into 2 Groups, Group I (n=15) samples and Group II (n=15) samples. The grouping was done based on the size of the lesion. Group I consisted of lesions of size greater than 5mm and group II consisted of lesions of size less than 5mm. the collected samples were then preserved. Because of the superior preservation of morphology, formalin- fixed paraffin-embedded (FFPE) tissue remains today the medium of choice for most clinical and research studies. The collected tissue specimens were fixed with 10% buffered formalin overnight and dehydrated in an ascending series of graded alcohol. Finally the fixed, dehydrated specimens were embedded in paraffin and made in to blocks. 5 micron thin sections were made from the paraffin blocks and the sections were transferred to the slides. The slides were processed immunohistochemically to locate the OSM antigen. Another 5 micron section from the samples were made and stained with eosin and hematoxylin to assess the magnitude of inflammation. The slides were then observed under light microscope at 40 X and graded. Results of the present showed that all the samples stained positive for OSM. Increased OSM expression was observed in group1 (i.e) lesions greater than 5 mm compared to smaller lesions. In addition increased OSM expression was observed in lesions showing high degree of inflammation. The results of the present study agree with the study performed by Tsai et al (2008) where OSM expression was increased with increase in the degree of inflammation. The OSM has received considerable attention because of its participation in many inflammatory diseases. OSM could be detected in areas of the chronic apical periodontitis lesions, suggesting that OSM, stored in the cytosol of epithelial cells, inflammatory, cell, fibroblasts, and endothelial cells, may represent a reservoir of OSM activity that can be released at certain stages of the inflammatory reaction. In addition, the expression of OSM increases with the grade of inflammation in apical periodontitis lesions. Thus the role of OSM in the pathogenesis of apical periodontitis lesion is worthy of further investigation. CONCLUSION: Within the limitations of the present study, it can be concluded that, (i) All the tissue specimens obtained from periapical surgery stained with anti OSM antibody showing the generalized presence of the OSM cytokine in cases with persistent periapical periodontitis. (ii) OSM forms the cytokine network that is responsible for the bone resorption associated with periapical lesions. (iii) Immunoreactivity of OSM was expressed in epithelium, endothelium, inflammatory infiltrates and fibroblasts. The OSM signal was expressed in the following rank order- inflammatory infiltrates (86.7%) > endothelium (73.3%) > epithelium (60%) > fibroblasts (23.3%). (iv) Increased OSM expression was observed in lesions greater than 5mm compared to smaller lesions. (v) Increased OSM expression was observed in lesions with increased degree of inflammation. (vi) Increase in OSM expression can denote the increase in degree of inflammation of periapical lesions.