RESUMO
BACKGROUND/PURPOSE: The relationship between endodontic and periodontal lesions remains a controversy. Their diagnosis is often difficult and requires an interdisciplinary approach to rule out the cause and provide appropriate treatment. Periodontitis as an etiology of pulpal necrosis and irreversible pulpitis has been a hypothetical concept. Thus, the aim of this study was to assess the non-carious teeth extracted due to periodontitis both clinically and histologically to understand the possible association between periodontitis and its effect on pulp vitality. MATERIALS AND METHODS: The study consisted of 60 teeth, of which 20 were extracted due to orthodontic requirements (control group) and 40 were extracted due to periodontitis (test group), which was further subclassified based on the presence or absence of gingival recession. Clinically, the teeth were categorized as non-vital after testing them with the electronic pulp tester (EPT). Later, these teeth were sectioned, and histopathological analysis was done to detect the presence of lateral or accessory canals. RESULTS: The results showed that there were mild to moderate deteriorative changes in the pulp in the periodontitis group without a gingival recession and moderate to severe changes in the pulp in the periodontitis group with a gingival recession. CONCLUSION: There exists a possible deteriorative effect on pulp vitality as a consequence of periodontitis, even when the vitality of the pulp remains unaffected by dental caries.
RESUMO
Introduction: Lactate dehydrogenase (LDH) is an enzyme seen within every cell during their normal metabolic function. It is always confined within the cell cytoplasm and it becomes extracellular only when a cell dies. The extracellular presence of LDH is related to cell necrosis and tissue breakdown. Therefore, we designed a study to estimate and compare LDH levels in the saliva of patients with oral cancer, oral leukoplakia (OL), and smokers without lesions and in controls. Materials and Methods: A total of 81 subjects of both genders, between the ages of 20 and 70 years, were included in the study. The study group was divided into four: group I-controls (n = 20), Group II-smokers (n = 20), Group III-subjects with OL (n = 20), and Group IV-subjects with oral squamous cell carcinoma (OSCC) (n = 21). Five milliliters of unstimulated salivary sample was collected from each participant, and salivary LDH level was measured. The obtained values were tabulated and statistically analyzed. P < 0.05 was considered to be statistically significant. Results: The difference in LDH levels among the four groups was found to "BE" statistically significant. LDH values showed a marked increase in the leukoplakia group (49.79 ± 19.88 IU/L) and OSCC group (106.97 ± 32.75 IU/L) when compared to controls and smokers. Conclusion: We found that salivary LDH was increased in patients with leukoplakia and OSCC. Smoking alone did not produce any alterations in salivary LDH. It is possible that salivary LDH could be a potential biomarker to identify early premalignant or malignant changes in smokers.
