Associations Between Structural and Social Determinants of Health With COVID Infection Rates at a Safety Net Hospital.

BACKGROUND:  The reported disproportionate impact of COVID-19 infections on minority populations may be due to living in disinvested communities with a high level of poverty, pollution, inadequate unsafe employment, and overcrowded housing. OBJECTIVE:  To determine the association of county, city, and individual risk factors with COVID-19 infection rates. METHODS:  Retrospective chart review on COVID-19 tests performed from March through July 2020 at Arrowhead Regional Medical Center (ARMC), Colton, California. RESULTS:  A total of 7104 tests were performed with 69% in the drive-through testing center. The mean duration of test-to-results time was 2.36 (+0.02) days. COVID-19 positive tests occurred in 1095 (15.4%). At least one symptom occurred in 414 (33%) with a sensitivity of 37.8, specificity of 86.02, a positive predictive value of 33.01, and a negative predictive value of 72.76. Individual factors significantly associated with testing positive for COVID-19 were diabetes, Hispanic ethnicity, and male gender. Younger age was significantly associated with testing COVID positive with the highest risk in children <10 years. COVID-19 positive persons significantly resided in cities with higher population density, household members, poverty, non-English speaking homes, disability, lower median household income, lack of health insurance and decreased access to a computer and Wi-Fi services. County health rankings showed a significant positive association between testing positive for COVID-19 with increased smoking, air pollution, violent crimes, physical inactivity, decreased education, and access to exercise.  Conclusion: Adverse county health rankings, socially and economically disadvantaged cities are associated with an increased risk of testing positive for COVD-19. This information can be used in strategic planning and invention mitigation.

DSPP dosage affects tooth development and dentin mineralization.

Dentin Sialoprotein (DSP) and phosphophoryn (PP) are two most dominant non-collagenous proteins in dentin, which are the cleavage products of the DSPP (dentin sialophosphoprotein) precursor protein. The absence of the DSPP gene in DSPP knock-out (KO) mice results in characteristics that are consistent with dentinogenesis imperfecta type III in humans. Symptoms include thin dentin, bigger pulp chamber with frequent pulp exposure as well as abnormal epithelial-mesenchymal interactions, and the appearance of chondrocyte-like cells in dental pulp. To better understand how DSPP influences tooth development and dentin formation, we used a bacterial artificial chromosome transgene construct (BAC-DSPP) that contained the complete DSPP gene and promoter to generate BAC-DSPP transgenic mice directly in a mouse DSPP KO background. Two BAC-DSPP transgenic mouse strains were generated and characterized. DSPP mRNA expression in BAC-DSPP Strain A incisors was similar to that from wild-type (wt) mice. DSPP mRNA expression in BAC-DSPP Strain B animals was only 10% that of wt mice. PP protein content in Strain A incisors was 25% of that found in wt mice, which was sufficient to completely rescue the DSPP KO defect in mineral density, since microCT dentin mineral density analysis in 21-day postnatal animal molars showed essentially identical mineral density in both strain A and wt mice. Strain B mouse incisors, with 5% PP expression, only partially rescued the DSPP KO defect in mineral density, as microCT scans of 21-day postnatal animal molars indicated a reduced dentin mineral density compared to wt mice, though the mineral density was still increased over that of DSPP KO. Furthermore, our findings showed that DSPP dosage in Strain A was sufficient to rescue the DSPP KO defect in terms of epithelial-mesenchymal interactions, odontoblast lineage maintenance, along with normal dentin thickness and normal mineral density while DSPP gene dosage in Strain B only partially rescued the aforementioned DSPP KO defect.

Dentin sialophosphoprotein: a regulatory protein for dental pulp stem cell identity and fate.

The dentin sialophosphoprotein (dspp) transcript is expressed during tooth development as a DSPP precursor protein, which then undergoes cleavage to form mature dentin sialoprotein (DSP) and phosphophoryn (PP) proteins. Previous studies using DSPP-knockout (KO) mice have reported that these animals have hypomineralized teeth, thin dentin, and a large dental pulp chamber, similar to those from patients with dentinogenesis imperfecta III. However, there is no information about factors that regulate dental pulp stem cell lineage fate, a critical early event in the odontoblast-dentin mineralization scheme. To reveal the role of DSPP in odontoblast lineage differentiation during tooth development, we systematically examined teeth from wild-type (wt) and DSPP-KO C57BL/6 mice between the ages of postnatal day 1 and 3 months. We found developmental abnormalities not previously reported, such as circular dentin formation within dental pulp cells and altered odontoblast differentiation in DSPP-KO mice, even as early as 1 day after birth. Surprisingly, we also identified chondrocyte-like cells in the dental pulp from KO-mice teeth. Thus, these studies that compare wt and DSPP-KO mice suggest that the expression of DSPP precursor protein is required for normal odontoblast lineage differentiation and that the absence of DSPP allows dental pulp cells to differentiate into chondrocyte-like cells, which could negatively impact pulpal wound healing and tissue regeneration.