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Comparative Study
. 2008 Nov-Dec;23(6):1071-81.

Factors influencing effects of specific COX-2 inhibitor NSAIDs on growth and differentiation of mouse osteoblasts on titanium surfaces

Affiliations
  • PMID: 19216276
Comparative Study

Factors influencing effects of specific COX-2 inhibitor NSAIDs on growth and differentiation of mouse osteoblasts on titanium surfaces

Premijt Arpornmaeklong et al. Int J Oral Maxillofac Implants. 2008 Nov-Dec.

Abstract

Purpose: To investigate the influence of exposure time and stages of cell growth on the effects of specific COX-2 inhibitor NSAIDs on growth and differentiation of osteoblasts on smooth titanium surfaces.

Materials and methods: The study was categorized into 5 groups: group A, 0.1 microM indomethacin; group B, 1.5 microM celecoxib; group C, 3.0 microM celecoxib; group D, 9.0 microM celecoxib; and group E, serum-free culture medium without drug treatment. A mouse calvarial cell line, MC3T3-E1, was seeded on acid-prickled surface titanium disks. The investigations were performed in 3 experimental phases based on stages of cell growth: static (24 hours after seeding), log (culture day 5), and plateau (culture day 12). In each experimental phase, cells on titanium disks were incubated in a medium treated with drugs according to the groups of study for 1, 3, and 5 days.

Results: Indomethacin and celecoxib in groups A to D inhibited growth of cells on treatment days 3 and 5 in static phase and on treatment day 3 in log phase. Additionally, an inhibitory effect of indomethacin was greater than celecoxib. Effects on alkaline phosphatase (ALP) activity and osteocalcin were not clearly demonstrated. A significant decrease of PGE2 production was found in groups A to D in static and plateau but not log phases.

Conclusion: A specific COX-2 inhibitor NSAID, celecoxib, inhibited growth of osteoblasts on titanium surfaces and the effects were influenced by exposure time and stages of cell growth. Using a specific COX-2 inhibitor might cause deterioration of osteointegration of dental implants by interfering with osteoblastic cell growth in the proliferative stage.

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