Bone remodeling is a cyclic and continuous physiological process, which ensures the conservation and renewal of the bone matrix. Osteosynthesis of the bone matrix is achieved by osteoblasts and coordinated within this complex machinery of bone remodeling with resorption of extracellular bone matrix performed by osteoclasts. The mismatch between the activities of osteoblasts and osteoclasts has immunopathologic implications associated with either a decrease or increase of bone mass mineral density. The balance of the trimolecular control factor complex composed of osteoprotegerin (OPG), RANKL (osteoprotegerin ligand) and RANK maintains physiologic bone remodeling. This trimolecular complex functions as receptors and ligands and belongs to the superfamily of tumor necrosis factor (TNF). This mini review highlights the complex interplay of the RANKL–RANK/OPG axis and their immunopathologic implications in clinical medicine.

Cleft lip and palate (CLP) are birth defects that affect the upper lip and the roof of the mouth. CLP has a multifactorial etiology, comprising both genetic and environmental factors. In this review we discuss the recent data on the etiology of cleft lip and palate. We conducted a search of the MEDLINE database (Entrez PubMed) from January 1986 to December 2010 using the key words: ‘cleft lip,’ ‘cleft palate,’ ‘etiology,’ and ‘genetics.’ The etiology of CLP seems complex, with genetics playing a major role. Several genes causing syndromic CLP have been discovered. Three of them—T-box transcription factor-22 (TBX22), poliovirus receptor-like-1 (PVRL1), and interferon regulatory factor-6 (IRF6)—are responsible for causing X-linked cleft palate, cleft lip/palate–ectodermal dysplasia syndrome, and Van der Woude and popliteal pterygium syndromes, respectively; they are also implicated in nonsyndromic CLP. The nature and functions of these genes vary widely, illustrating the high vulnerability within the craniofacial developmental pathways. The etiological complexity of nonsyndromic cleft lip and palate is also exemplified by the large number of candidate genes and loci. To conclude, although the etiology of nonsyndromic CLP is still largely unknown, mutations in candidate genes have been identified in a small proportion of cases. Determining the relative risk of CLP on the basis of genetic background and environmental influence (including smoking, alcohol use, and dietary factors) will be useful for genetic counseling and the development of future preventive measures.

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Objective: To compare the effectiveness of preoperative administration of ibuprofen and piroxicam on orthodontic pain experienced after separator placement. Materials and Methods: Ninety patients aged between 13 years 9 months and 18 years 2 months who were to undergo fixed appliance orthodontic treatment were enrolled in this double-blind, parallel-arm, prospective study. Patients were evenly and randomly distributed to any of three experimental groups, as follows: (1) administration of placebo, (2) administration of 400 mg ibuprofen, and (3) administration of 20 mg piroxicam; medications were administered 1 hour before separator placement. The pain perceived was recorded by the patients on a linear and graded Visual Analogue Scale at time intervals of 2 hours; 6 hours; nighttime on the day of appointment; 24 hours after the appointment; and 2 days, 3 days, and 7 days after separator placement during each of the four activities (viz, chewing, biting, fitting front teeth, and fitting back teeth). Results:The results revealed that preoperative administration of 20 mg of piroxicam 1 hour prior to separator placement resulted in a significant decrease in pain levels at 2 hours, 6 hours, nighttime, and 24 hours and on the second and third days after separator placement, compared to patients on a placebo or ibuprofen. Conclusions: Premedication with 20 mg of piroxicam results in significantly decreased pain experienced, compared to premedication with 400 mg of ibuprofen or placebo. Usage of 20 mg of piroxicam 1 hour prior to separator placement is recommended. (Angle Orthod. 2011;81:1097-1102

Aim:The aim of this in vitro study was to evaluate the influence of the Dental chair light on the bond strength of light cured composite resin.Materials and Methods:Sixty therapeutically extracted human premolar teeth were randomly allocated to two groups of 30 specimens each. In both groups light cured composite resin (Transbond XT) and MBT premolar metal brackets (3M Unitek) was used to bond brackets. In group I and II light curing was done using Light-emitting diode light curing units without and with the dental chair light respectively. After bonding, all samples were stored in distilled water at room temperature for 24 hours and subsequently tested for shear bond strength and Adhesive Remnant Index (ARI) scores. Data was subjected to Mann Whitney U statistical test.Results:Results indicated that there was significantly higher shear bond strength (7.71 ± 1.90) for the Group II (composite cured with LED and dental chair light) compared with Group I (composite cured with LED LCU only) (5.74 ± 1.13).the obtained difference was statistically significant. There was no statistical significant difference between ARI scores in between the groups.Conclusions:light cure bonding with dental chair light switched on will produce greater bond strength than the conventional bonding. However, the ARI score were similar to both the groups. It is advised that the inexperienced orthodontist should always switch off the dental chair light while bonding for enough working time during the bracket placement.