Arachidonic acid and prostaglandin E2 influence human osteoblast (MG63) response to titanium surface roughness.

David D Dean, Casey M. Campbell, Scott F. Gruwell, John W M Tindall, Hui Hsiu Chuang, Weinan Zhong, John P. Schmitz, Victor L. Sylvia

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Prior studies have shown that implant surface roughness affects osteoblast proliferation, differentiation, matrix synthesis, and local factor production. Further, cell response is modulated by systemic factors, such as 1,25(OH)2D3 and estrogen as well as mechanical forces. Based on the fact that peri-implant bone healing occurs in a site containing elevated amounts of prostaglandin E2 (PGE2), the hypothesis of the current study is that PGE2 and arachidonic acid (AA), the substrate used by cyclooxygenase to form PGE2, influence osteoblast response to implant surface roughness. To test this hypothesis, 4 different types of commercially pure titanium (cpTi) disks with surfaces of varying roughness (smooth Ti, R(a) 0.30 microm; smooth and acid etched Ti [SAE Ti], R(a) 0.40 microm; rough Ti, R(a) 4.3 microm; rough and acid etched Ti [RAE Ti], R(a) 4.15 (microm) were prepared. MG63 osteoblasts were seeded onto the surfaces, cultured to confluence, and then treated for the last 24 hours of culture with AA (0, 0.1, 1, and 10 nM), PGE2 (0, 1, 10, 25, and 100 nM), or the general cyclooxygenase inhibitor indomethacin (0 or 100 nM). At harvest, the effect of treatment on cell proliferation was assessed by measuring cell number and [3H]-thymidine incorporation, and the effect on cell differentiation was determined by measuring alkaline phosphatase (ALP) specific activity. The effect of AA and PGE2 on cell number was somewhat variable but showed a general decrease on plastic and smooth surfaces and an increase on rough surfaces. In contrast, [3H]-thymidine incorporation was uniformly decreased with treatment on all surfaces. ALP demonstrated the most prominent effect of treatment. On smooth surfaces, AA and PGE2 dose-dependently increased ALP, while on rough surfaces, treatment dose-dependently decreased enzyme specific activity. Indomethacin treatment had either no effect or a slightly inhibitory effect on [3H]-thymidine incorporation on all surfaces. In contrast, indomethacin inhibited ALP on smooth surfaces and stimulated ALP on rough. Taken together, the results indicate that both AA and PGE2 influence osteoblast response by promoting osteoblast differentiation on smooth surfaces, while inhibiting it on rough surfaces. Because implants with rough surfaces are acknowledged to be superior to those with smooth surfaces, these results suggest that use of nonsterioidal anti-inflammatory drugs to block PGE2 production and reduce inflammation may be beneficial in the postoperative period after implant placement. They also indicate that manipulation of the AA metabolic pathway may offer a new therapeutic approach for modulating bone healing after implant placement. Because peri-implant healing takes place in a complex cellular environment quite different from the one used in the present study, additional work will be necessary to substantiate these possibilities.

Original languageEnglish (US)
Pages (from-to)303-312
Number of pages10
JournalThe Journal of oral implantology
Volume34
Issue number6
DOIs
StatePublished - 2008

Fingerprint

Titanium
Osteoblasts
Dinoprostone
Arachidonic Acid
Alkaline Phosphatase
Indomethacin
Thymidine
Therapeutics
Cell Count
Bone and Bones
Acids
Cyclooxygenase Inhibitors
Prostaglandin-Endoperoxide Synthases
Metabolic Networks and Pathways
Postoperative Period
Plastics
Cell Differentiation
Estrogens
Anti-Inflammatory Agents
Cell Proliferation

ASJC Scopus subject areas

  • Oral Surgery

Cite this

Dean, D. D., Campbell, C. M., Gruwell, S. F., Tindall, J. W. M., Chuang, H. H., Zhong, W., ... Sylvia, V. L. (2008). Arachidonic acid and prostaglandin E2 influence human osteoblast (MG63) response to titanium surface roughness. The Journal of oral implantology, 34(6), 303-312. https://doi.org/10.1563/1548-1336-34.6.303

Arachidonic acid and prostaglandin E2 influence human osteoblast (MG63) response to titanium surface roughness. / Dean, David D; Campbell, Casey M.; Gruwell, Scott F.; Tindall, John W M; Chuang, Hui Hsiu; Zhong, Weinan; Schmitz, John P.; Sylvia, Victor L.

In: The Journal of oral implantology, Vol. 34, No. 6, 2008, p. 303-312.

Research output: Contribution to journalArticle

Dean, DD, Campbell, CM, Gruwell, SF, Tindall, JWM, Chuang, HH, Zhong, W, Schmitz, JP & Sylvia, VL 2008, 'Arachidonic acid and prostaglandin E2 influence human osteoblast (MG63) response to titanium surface roughness.', The Journal of oral implantology, vol. 34, no. 6, pp. 303-312. https://doi.org/10.1563/1548-1336-34.6.303
Dean, David D ; Campbell, Casey M. ; Gruwell, Scott F. ; Tindall, John W M ; Chuang, Hui Hsiu ; Zhong, Weinan ; Schmitz, John P. ; Sylvia, Victor L. / Arachidonic acid and prostaglandin E2 influence human osteoblast (MG63) response to titanium surface roughness. In: The Journal of oral implantology. 2008 ; Vol. 34, No. 6. pp. 303-312.
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