Gingival overgrowth caused by Olmesartan Medoxomil: Observational study

Objective: Olmesartan Medoxomil is a type 1 receptor antagonist an antagonist of type 1 receptor (AT1) of angiotensin II (A-II) that inhibits numerous actions of A-II in the renin-angiotensin-aldosterone system (RAAS). A-II is a significant and multifunctional peptide involved in the pathophysiology of blood hypertension and for this reason it represents the main target in several classes of drugs used to treat and control arterial hypertension, such as angiotensin converting enzyme inhibitors (ACE-i), angiotensin receptor blockers (ARB) and renin direct inhibitors. The aim of the study is to evaluate whether the two drugs that have as an active principle Olmesartan Medoxomil, with and without the diuretic hydrochlorothiazide, are able to determine gingival overgrowth. Study Design: 108 subjects were examined and divided into three groups: G1, subjects treated with Olmesartan Medoxomil and hydrochlorothiazide (n=60); G2, subjects received only Olmesartan Medoxomil (n=24); G3, control group without pharmacological therapies (n=24). The plaque index (IP) and the gingival overgrowth index (OI) were recorded, considering the vertical and horizontal components. Results: Vertical overgrowth averaged between 0.17 \ub1 0.15 (G3) and 0.34 \ub1 0.26 (G2) showing statistically significant differences (p <0.05) compared to the other groups. Horizontal overgrowth ranged from 0.18 \ub1 0.26 (G3) to 0.49 \ub1 0.35 (G2) showing statistically significant differences (p <0.05). Conclusions: antihypertensive agents as Olmesartan Medoxomil may result in mild gingival overgrowth in the upper and lower frontal dental elements not related to other etiological factors

Efficacy of two dosages of dexamethasone administered by submucosal injection on postoperative sequelae after third molar surgery: A retrospective study

ABSTRACT: Purpose: A retrospective clinical study was performed to compare the post-operative sequelae of the submucosal administration of two different low dosages of dexamethasone, after the surgical extraction of lower third molars. Methods: Data regarding edema, trismus, pain and analgesic consumption were collected from 150 subjects, selecting three equal groups (n= 50): a control group with no administered dexamethasone (G1); submucosal injection of dexamethasone 2 mg/0.5 ml (G2) and submucosal injection of dexamethasone 4 mg/1 ml (G3). Collected data were evaluated at three different time points: T0 before surgery, T1 on the third day after surgery and T2 on the 7th day after surgery. Patients’ gender and age were also considered for statistical purposes. Results: The effects on facial swelling reduction were statistically significant in G2 at T1 in the male subgroup. With trismus, the differences between the time points considered were statistically significant in G2 in the subgroup of subjects younger than 25 years old. Differences in analgesics taken were statistically significant when G1 and G2 were compared at T1. (Am J Dent 2022;35:233-237)

Perinatal triphenyl phosphate exposure accelerates type 2 diabetes onset and increases adipose accumulation in UCD-type 2 diabetes mellitus rats

Triphenyl phosphate (TPhP) is a flame retardant additive frequently found in consumer products and household dust. We administered 170 μg of TPhP in maternal food from gestational day 8.5 to weaning and evaluated metabolic phenotypes of 3.5 month old male and female rats, and weight-matched males up to 6 months, to assess the development of obesity and type 2 diabetes mellitus (T2DM), respectively. Perinatal TPhP exposure increased body and fat mass in 3.5 month old male and female rats, while leptin and cumulative energy intake were elevated in males and females, respectively. Independent of body mass, perinatal TPhP exposure accelerated T2DM onset in males and increased plasma non-esterified- fasting fatty acids. These observations suggest that perinatal exposure to TPhP exacerbates the development of obesity in male and female UCDavis-T2DM rats and accelerates T2DM onset in male UCD-T2DM rats