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Biomedical subjects

M D Henry

Publications and source records attributed to M D Henry.

20 records · Page 2Linked to original sources

Avoiding implant overload.

Implant overload can be caused by a great number of factors, including suboptimal implant design and size; an insufficient number of implants to support the restoration; improperly splinted abutments; violation of conventional prosthetic limitations for natural dentition; excessively cantilevered pontics; splinting to natural dentition, even with a stress-breaking attachment; improperly positioned implants; the wrong type of restoration for the clinical condition; loss of supporting bone; excessive parafunctional forces; and non-maintenance of the components. Screws loosening or crestal bone loss are frequently the first detectable signs of implant overload, and warrant immediate action. Other signs of occlusal overload include infection, inflammation and peri-implant radiolucency. Balancing the whole arch, reducing contacts and surface area of the implant-supported areas, and shortening or eliminating cantilevers whenever possible are initial steps that can be taken to eliminate or lessen the excessive stress. The strongest possible implant and restorative materials should be used, and the patient should also be instructed as to proper implant function. As oral implantology develops at a seemingly exponential rate, it is extremely important to keep abreast of the latest advancements. Overload, rather than component design, is the primary factor in the majority of prosthetic and implant failures. Safeguarding the long-term integrity of the restoration should be a shared responsibility involving the patient and the health care team.

Dental Abutments↗

Role of the heat shock response in stability of mRNA in Escherichia coli K-12.

The heat shock response in Escherichia coli involves extensive induction of the heat shock proteins, with the concomitant suppression of the synthesis of the non-heat shock proteins. While the induction of the heat shock proteins has been shown to occur primarily at the transcriptional level, the suppression of non-heat shock proteins is poorly understood. We have investigated the possibility that an increased decay of non-heat shock mRNAs is a means of decreasing the synthesis of non-heat shock proteins during the heat shock response. Heat shock response-defective strains were compared with wild-type controls by several criteria to evaluate both mRNA stability and the induction of enzymes known to be involved in mRNA turnover. Our results indicate that increased mRNA decay is not a mechanism used to regulate the synthesis of non-heat shock proteins.

Bacterial Proteins↗