The normative values for resting length of pectoralis minor muscle among individuals with asymptomatic shoulder in South Bengaluru: a cross-sectional pilot study.

OBJECTIVE: The aim of the study was to determine the normative values for resting length of pectoralis minor muscle among males and females with an asymptomatic shoulder in South Bengaluru. PATIENTS AND METHODS: Two hundred and forty-six subjects with asymptomatic shoulders were taken by convenience sampling. The subjects were divided into two groups: Group A (123 males) and Group B (123 females). Pectoralis minor muscle resting length was measured on their dominant side in all subjects. Post measurement, the PMI was calculated. The normative values for both groups were determined. The mean PMI was compared between Group A and Group B and was analyzed using statistical tools. RESULTS: In Group A, the mean average Pectoralis minor length (PML) was 14.59 ± 1.61 cm and in Group B, the mean average PML was 12.95 ± 1.42 cm which was statistically significant (p-value <0.00001). In Group A, the mean Pectoralis Minor Index (PMI) was 8.54 ± 0.88 and in Group B, the mean PMI was 8.22 ± 0.90 which was statistically significant (p-value <0.005). CONCLUSIONS: The normative values for resting length of pectoralis minor muscle for males are 8.54 ± 0.88 and for females 8.22 ± 0.90 with an asymptomatic shoulder. There is a difference in the normative values for the resting PML in the asymptomatic shoulder by gender.

Recessive oligodontia linked to a homozygous loss-of-function mutation in the SMOC2 gene.

OBJECTIVE: Recently, several genes have been reported with mutations or variants that underlie a number of syndromic and non-syndromic forms of oligodontia including MSX1, PAX9, AXIN2, EDA and WNT10A. This study aimed to identify the causal mutations in a consanguineous Pakistan family with oligodontia and microdontia. DESIGN: Exome sequencing was performed in two of affected members of the Pakistan family. RESULTS: The exome sequencing data revealed that the affected individuals were homozygous with a novel mutation in exon 8 of the SMOC2 gene, c.681T>A (p.C227X). CONCLUSIONS: This is the second report describing SMOC2 mutations with oligodontia and microdontia underlining the key role for this signalling molecule in tooth development.