Mutations in these connexins lead to absent or malformed gap junctions and congenital deafness.
In addition, the adjacent teeth might have erupted into the gaps, camouflaging the congenital absence of one or more teeth.
Although these are all laudable aims, the work presented here shows that unless interventions target specifically the risk of very premature birth and potentially lethal congenital abnormalities the effect on the deprivation gap is likely to be minor.
By contrast, immaturity and congenital anomalies accounted for 53% of the deprivation gap in 1997-9, whincreasedased to 73% in 2003, similar to the percentage seen for neonatal mortality.
Regardless, developmental abnormalities of Kölliker's organ may lead to congenital hearing loss, considering that mutations in ion channels (hemichannels, gap junctions, and calcium channels) involved in Kölliker's organ activity share strong links with such types of deafness.
In many developing countries, birth defects registries are absent and the health care services, from antenatal through obstetric to postnatal and adolescent health care, are challenged with fundamental gaps in the understanding, prevention, and treatment of congenital anomalies.
Wide deprivation gaps were also seen for deaths due to congenital anomalies (RR 2.8, 95% CI 2.4 to 3.3) and maternal disorders such as hypertension (RR 2.2, 95% CI 1.9 to 2.5).
For congenital anomalies, immaturity, and accidents and other specific causes, the relative deprivation gap widened between 1997-9 and 2003-5, before a slight fall in 2006-7.
Current recommendations for molecular diagnostic testing of patients with congenital hearing loss advise to first test the GJB2 gene that encodes the gap junction protein connexin 26.
Conclusions Almost 80% of the relative deprivation gap in all cause mortality was explained by premature birth and congenital anomalies.
