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David L. Cochran

Researcher at University of Texas Health Science Center at San Antonio

Publications -  77
Citations -  10348

David L. Cochran is an academic researcher from University of Texas Health Science Center at San Antonio. The author has contributed to research in topics: Osseointegration & Implant. The author has an hindex of 44, co-authored 77 publications receiving 10048 citations. Previous affiliations of David L. Cochran include Boston University & Virginia Commonwealth University.

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Effect of titanium surface roughness on proliferation, differentiation, and protein synthesis of human osteoblast-like cells (MG63)

TL;DR: It is demonstrated that surface roughness alters osteoblast proliferation, differentiation, and matrix production in vitro and suggests that implant surfaceroughness may play a role in determining phenotypic expression of cells in vivo.
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Response of MG63 osteoblast-like cells to titanium and titanium alloy is dependent on surface roughness and composition.

TL;DR: In this article, the effect of chemical composition and surface roughness of commercially pure titanium (Ti) and Ti-6A1-4V alloy (Ti-A) on MG63 osteoblast-like cells was investigated.
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Bone response to unloaded and loaded titanium implants with a sandblasted and acid-etched surface : A histometric study in the canine mandible

TL;DR: Results are consistent with earlier studies on SLA implants and suggest that this surface promotes greater osseous contact at earlier time points compared to TPS-coated implants.
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Surface roughness modulates the local production of growth factors and cytokines by osteoblast-like MG-63 cells.

TL;DR: Surface roughness affects cytokine and growth factor production by MG-63 cells, suggesting that surface roughness may modulate the activity of cells interacting with an implant, and thereby affect tissue healing and implant success.
Journal Article

IL-1 and TNF Antagonists Inhibit the Inflammatory Response and Bone Loss in Experimental Periodontitis

TL;DR: It is suggested that multiple pathologies involving excessive loss of bone may operate through a common mechanism involving IL-1 and/or TNF, and inflammation associated with gingivitis is actively protective, since blocking further up-regulation of the host response withIL-1/TNF inhibitors does not cause periodontal damage.