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1.
Arch Oral Biol ; 80: 136-143, 2017 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-28414988

RESUMEN

OBJECTIVE: The adaptation capacities of the mandibular condyle in response to mechanical stimuli might be different between juveniles and adults, but has not been compared. This study aimed to investigate whether abnormal molar occlusion and subsequent molar extraction could lead to different remodeling responses in the mandibular condyles of juvenile and adult rats. METHODS: Abnormal molar occlusion (AMO) was established in the 5- and 16-wk old rats by moving their maxillary left and mandibular right third molars distally. AMO was removed in the molar extraction group at 4 weeks but remained in the AMO group. All rats were sacrificed at 8 weeks. Micro-computed tomography, histomorphology, immunohistochemistry and real-time PCR were adopted to evaluate the remodeling of condylar subchondral bone. RESULTS: Condylar subchondral bone loss and increased osteoclastic activities were observed in both juvenile and adult AMO groups, while increased osteoblastic activities were only seen in the juvenile AMO group. Decreased bone mineral density, bone volume fraction and trabecular thickness, but increased trabecular separation, number and surface of osteoclasts and mRNA levels of TRAP, cathepsin-K, RANKL in the juvenile AMO group were all reversed after molar extraction (all P<0.05). However, these parameters showed no difference between adult AMO and extraction groups (all P>0.05). CONCLUSIONS: Abnormal molar occlusion led to degenerative remodeling in the mandibular condyles of both juvenile and adult rats, while exemption of abnormal occlusion caused significant rescue of the degenerative changes only in the juvenile rats.


Asunto(s)
Remodelación Ósea/fisiología , Maloclusión/fisiopatología , Cóndilo Mandibular/fisiopatología , Animales , Femenino , Inmunohistoquímica , Osteoblastos/fisiología , Osteoclastos/fisiología , Ratas , Ratas Sprague-Dawley , Reacción en Cadena en Tiempo Real de la Polimerasa , Microtomografía por Rayos X
2.
Sci Rep ; 6: 30085, 2016 07 25.
Artículo en Inglés | MEDLINE | ID: mdl-27452863

RESUMEN

This study tested whether activation of adrenoreceptors in chondrocytes has roles in degenerative remodelling of temporomandibular joint (TMJ) and to determine associated mechanisms. Unilateral anterior crossbite (UAC) was established to induce TMJ degeneration in rats. Saline vehicle, α2- and ß-adrenoreceptor antagonists or agonists were injected locally into the TMJ area of UAC rats. Cartilage degeneration, subchondral bone microarchitecture and the expression of adrenoreceptors, aggrecans, matrix metalloproteinases (MMPs) and RANKL by chondrocytes were evaluated. Chondrocytes were stimulated by norepinephrine to investigate signal transduction of adrenoreceptors. Increased α2A-adrenoreceptor expression was observed in condylar cartilage of UAC rats, together with cartilage degeneration and subchondral bone loss. Norepinephrine depresses aggrecans expression but stimulates MMP-3, MMP-13 and RANKL production by chondrocytes through ERK1/2 and PKA pathway; these effects were abolished by an α2A-adrenoreceptor antagonist. Furthermore, inhibition of α2A-adrenoreceptor attenuated degenerative remodelling in the condylar cartilage and subchondral bone, as revealed by increased cartilage thickness, proteoglycans and aggrecan expression, and decreased MMP-3, MMP-13 and RANKL expressions in cartilage, increased BMD, BV/TV, and decreased Tb.Sp in subchondral bone. Conversely, activation of α2A-adrenoreceptor intensified aforementioned degenerative changes in UAC rats. It is concluded that activation of α2A-adrenergic signal in chondrocytes promotes TMJ degenerative remodelling by chondrocyte-mediated pro-catabolic activities.


Asunto(s)
Condrocitos/metabolismo , Osteoartritis/patología , Receptores Adrenérgicos alfa 2/metabolismo , Transducción de Señal/efectos de los fármacos , Articulación Temporomandibular/metabolismo , Articulación Temporomandibular/patología , Agonistas Adrenérgicos/farmacología , Antagonistas Adrenérgicos/farmacología , Agrecanos/biosíntesis , Animales , Células Cultivadas , Activación Enzimática/efectos de los fármacos , Femenino , Cóndilo Mandibular/fisiología , Metaloproteinasas de la Matriz/biosíntesis , Norepinefrina/farmacología , Ligando RANK/biosíntesis , Ratas , Ratas Sprague-Dawley , Receptores Adrenérgicos beta/biosíntesis , Articulación Temporomandibular/citología
3.
Sci Rep ; 5: 12593, 2015 Jul 29.
Artículo en Inglés | MEDLINE | ID: mdl-26219508

RESUMEN

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 ß-adrenergic receptors (ß-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 ß-ARs, pro-osteoclastic gene expressions and pro-osteoclastic function. Increases in norepinephrine level, sympathetic nerve fiber distribution and ß2-AR expression were observed in the condylar subchondral bone of experimental rats, together with subchondral bone loss and increased osteoclast activity. ß-antagonist (propranolol) suppressed subchondral bone loss and osteoclast hyperfunction while ß-agonist (isoproterenol) exacerbated those responses. MSCs from experimental condylar subchondral bone expressed higher levels of ß2-AR and RANKL; norepinephrine stimulation further increased their RANKL expression and pro-osteoclastic function. These effects were blocked by inhibition of ß2-AR or the PKA pathway. RANKL expression by MSCs decreased after propranolol administration and increased after isoproterenol administration. It is concluded that ß2-AR signal-mediated subchondral bone loss in TMJ osteoarthritisis associated with increased RANKL secretion by MSCs.


Asunto(s)
Resorción Ósea/metabolismo , Huesos/metabolismo , Osteoartritis/metabolismo , Receptores Adrenérgicos beta/metabolismo , Transducción de Señal/fisiología , Articulación Temporomandibular/metabolismo , Adrenérgicos/farmacología , Animales , Remodelación Ósea/efectos de los fármacos , Remodelación Ósea/fisiología , Resorción Ósea/patología , Huesos/efectos de los fármacos , Huesos/patología , Femenino , Células Madre Mesenquimatosas/efectos de los fármacos , Células Madre Mesenquimatosas/metabolismo , Células Madre Mesenquimatosas/patología , Norepinefrina/farmacología , Osteoartritis/patología , Osteoclastos/efectos de los fármacos , Osteoclastos/metabolismo , Osteoclastos/patología , Ligando RANK/metabolismo , Ratas , Ratas Sprague-Dawley , Transducción de Señal/efectos de los fármacos , Articulación Temporomandibular/efectos de los fármacos , Articulación Temporomandibular/patología
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