Closure of Alveolar Cleft by Iliac Bone Grafting: a Case Report

Introduction: Orofacial clefts are the most common craniofacial birth defects, affecting a significant number of individuals worldwide. The alveolar cleft is a developmental defect that affects the alveolar process of the maxilla and is often associated with cleft lip and palate. Methods: In this case report, we present the case of a 20-year-old female patient with alveolar cleft who underwent secondary alveolar cleft reconstruction using autologous iliac bone grafting. The aim of the procedure was to restore the function and form of the maxillary arch, facilitate ridge augmentation for further prosthetic rehabilitation, repair the nasal floor, and facilitate orthodontic treatment. Results: The procedure was successful in achieving the desired outcomes, and the patient's occlusal relationship was improved. Additionally, the alar base symmetry was enhanced, and speech was improved. Conclusion: Alveolar cleft reconstruction using autologous iliac bone grafting is a successful approach to treating alveolar clefts. The procedure can restore the form and function of the maxillary arch and facilitate further prosthetic rehabilitation and orthodontic treatment. The effectiveness of the procedure should be monitored closely to ensure optimal outcomes. Update Dent. Coll. j: 2023; 13(1): 35-3

Elevated concentrations of serum matrix metalloproteinase-2 and -9 and their associations with circulating markers of cardiovascular diseases in chronic arsenic-exposed individuals

Background: Cardiovascular diseases (CVDs) and cancers are the major causes of chronic arsenic exposure-related morbidity and mortality. Matrix metalloproteinase-2 (MMP-2) and −9 (MMP-9) are deeply involved in the pathogenesis of CVDs and cancers. This study has been designed to evaluate the interactions of arsenic exposure with serum MMP-2 and MMP-9 concentrations especially in relation to the circulating biomarkers of CVDs. Methods: A total of 373 human subjects, 265 from arsenic-endemic and 108 from non-endemic areas in Bangladesh were recruited for this study. Arsenic concentrations in the specimens were measured by inductively coupled plasma mass spectroscopy (ICP-MS) and serum MMPs were quantified by immunoassay kits. Results: Serum MMP-2 and MMP-9 concentrations in arsenic-endemic population were significantly (p < 0.001) higher than those in non-endemic population. Both MMPs showed significant positive interactions with drinking water (rs = 0.208, p < 0.001 for MMP-2; rs = 0.163, p <0.01 for MMP-9), hair (rs= 0.163, p < 0.01 for MMP-2; rs = 0.173, p < 0.01 for MMP-9) and nail (rs= 0.160, p < 0.01 for MMP-2; rs = 0.182, p < 0.001 for MMP-9) arsenic of the study subjects. MMP-2 concentrations were 1.02, 1.03 and 1.05 times, and MMP-9 concentrations were 1.03, 1.06 and 1.07 times greater for 1 unit increase in log-transformed water, hair and nail arsenic concentrations, respectively, after adjusting for covariates (age, sex, BMI, smoking habit and hypertension). Furthermore, both MMPs were increased dose-dependently when the study subjects were split into three (≤10, 10.1-50 and > 50 μg/L) groups based on the regulatory upper limit of water arsenic concentration set by WHO and Bangladesh Government. MMPs were also found to be significantly (p < 0.05) associated with each other. Finally, the concentrations of both MMPs were correlated with several circulating markers related to CVDs. Conclusions: This study showed the significant positive associations and dose–response relationships of arsenic exposure with serum MMP-2 and MMP-9 concentrations. This study also showed the interactions of MMP-2 and MMP-9 concentrations with the circulating markers of CVDs suggesting the MMP-2 and MMP-9 -mediated mechanism of arsenic-induced CVDs

Association between arsenic exposure and soluble thrombomodulin: A cross sectional study in Bangladesh

<div><p>Chronic exposure to arsenic is associated with increased morbidity and mortality from cardiovascular disease (CVD); however, plausible biomarker for early prediction and the underlying mechanism of arsenic-related CVD have not yet been clearly understood. Endothelial dysfunction plays a central role in the development of CVD. We hypothesized that endothelial damage or dysfunction is an important aspect and may be an early event of arsenic-related CVD. Soluble thrombomodulin (sTM) in serum is thought to be a specific and stable marker for endothelial damage or dysfunction. This study was designed to evaluate the association between chronic exposure to arsenic and sTM among human subjects in arsenic-endemic and non-endemic rural areas in Bangladesh. A total of 321 study subjects (217 from arsenic-endemic areas and 104 from a non-endemic area) were recruited. Subjects’ arsenic exposure levels (i.e., drinking water, hair and nail arsenic concentrations) were measured by Inductively Coupled Plasma Mass Spectroscopy. The subjects’ serum sTM levels were quantified by immunoassay kit. The average sTM levels of the subjects in arsenic-endemic and non-endemic areas were 4.58 ± 2.20 and 2.84 ± 1.29 (ng mL^-1) respectively, and the difference was significant (<i>p</i><0.001). Arsenic exposure levels showed a significant (water arsenic: <i>r</i>_<i>s</i> = 0.339, <i>p</i><0.001, hair arsenic: <i>r</i>_<i>s</i> = 0.352, <i>p</i><0.001 and nail arsenic: <i>r</i>_<i>s</i> = 0.308, <i>p</i><0.001) positive associations with sTM levels. Soluble TM levels were higher in the higher exposure gradients if we stratified the subjects into tertile groups (low, medium and high) based on the arsenic concentrations of the subjects’ drinking water, hair and nails. Finally, increased levels of sTM were negatively correlated with high density lipoprotein cholesterol (HDL-C), and positively correlated with intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). Results of this study show that chronic exposure to arsenic has mild to moderate association with sTM levels.</p></div

Associations of arsenic exposure and other variables with sTM levels through multiple linear regression analyses.

<p>Associations of arsenic exposure and other variables with sTM levels through multiple linear regression analyses.</p

Dose-response relationship between arsenic exposure and sTM levels.

<p>Data were presented as mean ± SE. Dose-response relationship between arsenic exposure and sTM levels in one-way ANOVA was examined by F-test, followed by Bonferroni multiple comparison test between each group of exposure level. Arsenic concentrations in water: low (0.03–5.22 μg L^-1; n = 101), medium (5.30–127.00 μg L^-1; n = 110), and high (129.00–546.00 μg L^-1; n = 110). Arsenic concentration in hair: low (0.02–0.62 μg g^-1; n = 106), medium (0.64–3.36 μg g^-1; n = 106), and high (3.40–37.24 μg g^-1; n = 109). Arsenic concentrations in nail: low (0.15–2.12 μg g^-1; n = 104), medium (2.14–7.45 μg g^-1; n = 109), and high (7.45–37.42 μg g^-1; n = 108). ^a and ^b, Significant from low and medium groups, respectively. ***<i>p</i> < 0.001; **<i>p</i> < 0.01; *<i>p</i> < 0.05.</p

Interaction between exposure and hypertension on sTM levels through univariate regression analyses.

<p>Interaction between exposure and hypertension on sTM levels through univariate regression analyses.</p

Association between arsenic exposure and serum sTM levels.

<p>Log₁₀-transformed values of water (μg L^-1), hair (μg g^-1), and nail (μg g^-1) arsenic concentrations were used. <i>r</i>_<i>s</i> and <i>p</i>-values were from Spearman correlation coefficient test.</p