RESUMO
BACKGROUND: The potential risk of coronavirus disease 2019 (COVID-19) transmission from asymptomatic COVID-19 patients is a concern in dental practice. However, the impact of this risk is not well documented to date. This report describes our dental clinical experience with patients who did not exhibit symptoms of COVID-19 but were later confirmed as positive for COVID-19. CASE PRESENTATION: Of the 149,149 patients who visited the outpatient clinic of KNUDH and the 3291 patients who visited the Oral and Maxillofacial Surgery Clinic of KNUH, 3 were later confirmed as having COVID-1 between 1 February 2020 and 28 February 2021. Owing to close contact with these patients during their treatments, 46 dental and medical staff had to undergo quarantine from the date of the patients' confirmation of COVID-19 infection. CONCLUSION: The presented cases showed the potential existence of asymptomatic COVID-19 patients after dental treatment with aerosol-generating procedures. Clinicians should be aware of the infection prevention measures and try to protect healthcare personnel from secondary infection of COVID-19 during dental treatments.
RESUMO
The zinc transporter protein ZIP13 plays critical roles in bone, tooth, and connective tissue development, and its dysfunction is responsible for the spondylocheirodysplastic form of Ehlers-Danlos syndrome (SCD-EDS, OMIM 612350). Here, we report the molecular pathogenic mechanism of SCD-EDS caused by two different mutant ZIP13 proteins found in human patients: ZIP13(G64D), in which Gly at amino acid position 64 is replaced by Asp, and ZIP13(ΔFLA), which contains a deletion of Phe-Leu-Ala. We demonstrated that both the ZIP13(G64D) and ZIP13(ΔFLA) protein levels are decreased by degradation via the valosin-containing protein (VCP)-linked ubiquitin proteasome pathway. The inhibition of degradation pathways rescued the protein expression levels, resulting in improved intracellular Zn homeostasis. Our findings uncover the pathogenic mechanisms elicited by mutant ZIP13 proteins. Further elucidation of these degradation processes may lead to novel therapeutic targets for SCD-EDS.