The aim of this study evaluate the salivary alkaline phosphatase levels in tobacco users to determine its role as a biomarker in oral potentially malignant disorders. This prospective observational study comprised 60 individuals aged between 18 and 70 years who were categorized into four   groups. For Group II, Group III and Group IV, individuals with the habit of smoking/tobacco chewing for a minimum period of 6 months were included in this study.  The mean values for S‑ALP were found to be about 19.00 IU/L (SD 12.37) for Group I (range from 7 to 50 IU/L), 8.50 IU/L (SD 3.35) for Group II (range from 2 to 14 IU/L), 5.60 IU/L (SD 1.01) for Group III (range from 1 to 8 IU/L) and 65.90 IU/L (SD 50.70) for Group IV (range from 10 to 146 IU/L). Comparison of S‑ALP between the groups showed a statistically significant difference (P < 0.001) using Kruskal–Wallis’ ANOVA. To know if there is any difference in S‑ALP levels between tobacco users and nonusers (Groups I and II and Groups I and III) and among the different forms of tobacco users (Groups II and III), the mean S‑ALP levels were compared using Mann–Whitney U‑test.

Gingival enlargement comprises any clinical condition in which an increase in the size of the gingiva is observed. It is a side effect associated with some distinct classes of drugs, such as anticonvulsants, immunosuppressant, and calcium channel blockers. Among calcium channel blockers, nifedipine causes gingival enlargement in about 10% of patients, whereas the incidence of amlodipine, a third-generation calcium channel blocker, induced gingival enlargement is very limited. Because the calcium antagonists, albeit to a variable degree, act as inhibitors of P-glycoprotein (P-gp), the gene product of multidrug resistance 1 (MDR1), and inflammation may modify P-gp expression. We hereby, report a case of amlodipine-induced gingival enlargement with MDR1 3435C/T polymorphism, associated with inflammatory changes due to plaque accumulation, in a 50-year-old hypertensive male patient. The genotype obtained for the polymorphism was a heteromutant genotype, thus supporting the contention that the MDR1 polymorphism may alter the inflammatory response to the drug.