β2-adrenergic signal transduction plays a detrimental role in subchondral bone loss of temporomandibular joint in osteoarthritis

Kai Jiao, Li Na Niu, Qi Hong Li, Gao Tong Ren, Chang Ming Zhao, Yun Dong Liu, Franklin Chi Meng Tay, Mei Qing Wang

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

The present study tested whether activation of the sympathetic tone by aberrant joint loading elicits abnormal subchondral bone remodeling in temporomandibular joint (TMJ) osteoarthritis. Abnormal dental occlusion was created in experimental rats, which were then intraperitoneally injected by saline, propranolol or isoproterenol. The norepinephrine contents, distribution of sympathetic nerve fibers, expression of β-adrenergic receptors (β-ARs) and remodeling parameters in the condylar subchondral bone were investigated. Mesenchymal stem cells (MSCs) from condylar subchondral bones were harvested for comparison of their β-ARs, pro-osteoclastic gene expressions and pro-osteoclastic function. Increases in norepinephrine level, sympathetic nerve fiber distribution and β2-AR expression were observed in the condylar subchondral bone of experimental rats, together with subchondral bone loss and increased osteoclast activity. β-antagonist (propranolol) suppressed subchondral bone loss and osteoclast hyperfunction while β-agonist (isoproterenol) exacerbated those responses. MSCs from experimental condylar subchondral bone expressed higher levels of β2-AR and RANKL; norepinephrine stimulation further increased their RANKL expression and pro-osteoclastic function. These effects were blocked by inhibition of β2-AR or the PKA pathway. RANKL expression by MSCs decreased after propranolol administration and increased after isoproterenol administration. It is concluded that β2-AR signal-mediated subchondral bone loss in TMJ osteoarthritisis associated with increased RANKL secretion by MSCs.

Original languageEnglish (US)
Article number12593
JournalScientific Reports
Volume5
DOIs
StatePublished - Jul 29 2015

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Temporomandibular Joint
Osteoarthritis
Adrenergic Agents
Signal Transduction
Bone and Bones
Mesenchymal Stromal Cells
Isoproterenol
Propranolol
Adrenergic Fibers
Norepinephrine
Osteoclasts
Nerve Fibers
Dental Occlusion
Bone Remodeling
Adrenergic Receptors
Joints
Gene Expression

ASJC Scopus subject areas

  • General

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β2-adrenergic signal transduction plays a detrimental role in subchondral bone loss of temporomandibular joint in osteoarthritis. / Jiao, Kai; Niu, Li Na; Li, Qi Hong; Ren, Gao Tong; Zhao, Chang Ming; Liu, Yun Dong; Tay, Franklin Chi Meng; Wang, Mei Qing.

In: Scientific Reports, Vol. 5, 12593, 29.07.2015.

Research output: Contribution to journalArticle

Jiao, Kai ; Niu, Li Na ; Li, Qi Hong ; Ren, Gao Tong ; Zhao, Chang Ming ; Liu, Yun Dong ; Tay, Franklin Chi Meng ; Wang, Mei Qing. / β2-adrenergic signal transduction plays a detrimental role in subchondral bone loss of temporomandibular joint in osteoarthritis. In: Scientific Reports. 2015 ; Vol. 5.
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abstract = "The present study tested whether activation of the sympathetic tone by aberrant joint loading elicits abnormal subchondral bone remodeling in temporomandibular joint (TMJ) osteoarthritis. Abnormal dental occlusion was created in experimental rats, which were then intraperitoneally injected by saline, propranolol or isoproterenol. The norepinephrine contents, distribution of sympathetic nerve fibers, expression of β-adrenergic receptors (β-ARs) and remodeling parameters in the condylar subchondral bone were investigated. Mesenchymal stem cells (MSCs) from condylar subchondral bones were harvested for comparison of their β-ARs, pro-osteoclastic gene expressions and pro-osteoclastic function. Increases in norepinephrine level, sympathetic nerve fiber distribution and β2-AR expression were observed in the condylar subchondral bone of experimental rats, together with subchondral bone loss and increased osteoclast activity. β-antagonist (propranolol) suppressed subchondral bone loss and osteoclast hyperfunction while β-agonist (isoproterenol) exacerbated those responses. MSCs from experimental condylar subchondral bone expressed higher levels of β2-AR and RANKL; norepinephrine stimulation further increased their RANKL expression and pro-osteoclastic function. These effects were blocked by inhibition of β2-AR or the PKA pathway. RANKL expression by MSCs decreased after propranolol administration and increased after isoproterenol administration. It is concluded that β2-AR signal-mediated subchondral bone loss in TMJ osteoarthritisis associated with increased RANKL secretion by MSCs.",
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