John C. Tiffee

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Postmenopausal osteoporosis, the most common bone disease in the developed world1, is associated with estrogen deficiency. This deficiency induces increased generation and activity of osteoclasts, which perforate bone trabeculae, thus reducing their strength and increasing fracture risk. Estrogen replacement prevents these effects2, indicating that estrogen(More)
Stress proteins (heat shock proteins [hsps]) serve a number of protective functions, including protection from apoptosis and acting as chaperones during protein biosynthesis. For example, hsp 27 has been defined as a chaperone for the G3 domain of aggrecan, while hsp 47 is the chaperone for type I collagen. Separate cytoprotective roles for hsp 27 and hsp(More)
c-src knockout and op/op mice develop osteopetrosis as a result of defective osteoclast function and osteoclast formation, respectively. The mutant mice can be distinguished readily from their wild-type littermates around 10–12 days after birth because their incisors do not erupt, but the morphology of their teeth and surrounding bone has not been reported(More)
Estrogen has been shown to protect osteoblastic cells from apoptosis. Similarly, estrogen treatment preceding heat shock elevates heat shock protein 27 (hsp27) expression and increases thermoresistance in the murine estrogen receptor-transformed SMER14 osteoblastic cell line. Forced expression of hsp27 expression in other cell lines limits apoptosis. The(More)
The vitality of teeth adjacent to dental implants should be considered in the treatment planning of dental implants. Both the restorability of an endodontically treated tooth and the risk of infection of the adjacent implant are important factors in planning for success. Given the illustrated difficulties and difficulties associated with resolving(More)
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