Role of CCR2 in orthodontic tooth movement

Taddei, Silvana Rodrigues de Albuquerque; Andrade, Ildeu; Queiroz-Junior, Celso Martins; Garlet, Thiago; Garlet, Gustavo; Cunha, Fernando; Teixeira, Mauro Martins; Silva, Tarcı́lia Aparecida

doi:10.1016/j.ajodo.2011.07.019

Cited by 69 publications

(40 citation statements)

References 30 publications

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“…23 These markers can act in some ways as macrophages or osteoclasts in the surrounding tissue of tooth. 27 Other markers have been related to local healing and activation of osteoclasts during orthodontic tooth movement. 28 These markers all help to amplify or maintain the inflammatory response and stimulation of the bone resorption machinery.…”

Section: Discussionmentioning

confidence: 99%

Periodontally Accelerated Molar Distalization With Miniscrew Assisted Memory Screw: A Pilot Study

Çörekçi¹,

Irgın²,

Halıcıoğlu³

et al. 2013

Turkish Journal of Orthodontics

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Objective: To examine the treatment effects of a miniscrew assisted memory screw system supported by piezoincision for the noncompliance molar distalization of maxillary first molars in patients with Class II malocclusion. Materials and Method: Nine subjects with skeletal Class I dental Class II malocclusion were treated. An anchorage unit was prepared using two miniscrew that were placed just behind a line connecting the first premolars at the mesial contact point. The memory expansion screw (500 g), and two miniscrews placed parallel to the occlusal plane provided stable, 4-point support for the appliance. Piezoincision was performed immediately after the appliance as cemented. Four midlevel incisions were made under local anesthesia between the roots of the teeth on the buccal side of the maxillary alveolar bone from the mesial first premolar to the second molar. A 3-mm piezoelectrical corticotomy was then performed by inserting the tip of Piezotome into each of these openings. Screw activation was started the following day. Skeletal and dental changes were measured on cephalograms, and dental casts were obtained before and after distalization. Results: Upper first molars were successfully distalized in approximately 4.6 months and the mean distalization at the end was 4.98 mm. The average distal tipping of the upper first molars was 7.758. No statistically significant changes were noted in the sagittal position of the maxilla or in the position of the upper incisors as a result of treatment. The maxillary first molars also moved palatinally (1.13 mm), but no significant distal rotation occurred. Conclusion: This system provided an efficient distalization method for posterior teeth and showed no anchorage loss. Molar tipping and palatal movement were observed as side effects in the patients. (Turkish J Orthod 2014;26:162-168)

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Section: Discussionmentioning

confidence: 99%

Periodontally Accelerated Molar Distalization With Miniscrew Assisted Memory Screw: A Pilot Study

Çörekçi¹,

Irgın²,

Halıcıoğlu³

et al. 2013

Turkish Journal of Orthodontics

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“…The number of mice per group was chosen based on a sample size estimation, 31,32 and this size has proven to yield reliable results in previous studies from our group using similar methodologies. 15,20,22,[33][34][35][36][37][38][39][40][41] Moreover, the experiment was repeated twice. On the 18th day after OVX, alveolar bone remodeling was induced by mechanical loading for 12 days.…”

Section: Animalsmentioning

confidence: 99%

ST2 regulates bone loss in a site‐dependent and estrogen‐dependent manner

Macari

Madeira

Lima

et al. 2018

J of Cellular Biochemistry

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Interleukin-33 (IL-33) and its receptor, ST2, are implicated in bone remodeling. The lack of estrogen after menopause results in an accelerated bone loss. Here we investigated the role of ST2 in the bone loss induced by estrogen deficiency. ST2-deficient mice (ST2 ) and their littermates (wildtype [WT]) were ovariectomized (OVX), while ovary-intact mice were used as controls. Bone sites were analyzed by microcomputed tomography, histomorphometry, and quantitative real-time polymerase chain reaction (qPCR). Deletion of IL-33 or ST2 resulted in a similar bone loss in the femur and maxilla. Ovariectomy in WT mice caused bone loss in the same areas. The lack of ST2 in OVX mice did not alter bone remodeling in the femur but prevented bone loss in the maxilla. Consistently, ovariectomy increased the IL-33 messenger RNA (mRNA) levels in the maxilla but not in the femur. Under mechanical stimulation, ovariectomy and ST2 deletion independently increased bone remodeling induced by orthodontic tooth movement, which was also associated with a greater number of osteoclasts and a reduced number of osteoblasts in the maxillary bone. ST2 OVX mice, however, displayed twice as many osteoblasts as that of WT OVX mice. Ovariectomy and ST2 deletion differently altered the cytokine mRNA levels in the maxilla. Remarkably, interleukin-10 expression was decreased in both WT OVX and ST2 mice, and this reduction was completely restored in ST2 OVX mice. The results demonstrate that estrogen and IL33/ST2 independently protect against bone loss. However, the ovariectomy-induced bone loss is IL-33/ST2-dependent in the maxilla but not in the femur, indicating a bimodal and site-specific role of ST2 in bone remodeling.

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“…CC chemokines Ligand 2 (CCL2) has been found to be involved in osteoclast activity and its expression is increased within the PDL on orthodontic force application. [19] There is a reduction of osteoclast and osteoblast activities in the absence of CCL2. Similarly CCR5 has been suggested to be a down regulator of alveolar bone resorption during orthodontic tooth movement.…”

Section: Inflammatory Mediators and Markers Of Alveolar Bone Remodellmentioning

confidence: 99%

Cellular response within the periodontal ligament on application of orthodontic forces

Meeran¹

2013

J Indian Soc Periodontol

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During application of controlled orthodontic force on teeth, remodeling of the periodontal ligament (PDL) and the alveolar bone takes place. Orthodontic forces induce a multifaceted bone remodeling response. Osteoclasts responsible for bone resorption are mainly derived from the macrophages and osteoblasts are produced by proliferations of the cells of the periodontal ligament. Orthodontic force produces local alterations in vascularity, as well as cellular and extracellular matrix reorganization, leading to the synthesis and release of various neurotransmitters, cytokines, growth factors, colony-stimulating factors, and metabolites of arachidonic acid. Although many studies have been reported in the orthodontic and related scientific literature, research is constantly being done in this field resulting in numerous current updates in the biology of tooth movement, in response to orthodontic force. Therefore, the aim of this review is to describe the mechanical and biological processes taking place at the cellular level during orthodontic tooth movement.

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Role of CCR2 in orthodontic tooth movement

Cited by 69 publications

References 30 publications

Periodontally Accelerated Molar Distalization With Miniscrew Assisted Memory Screw: A Pilot Study

Periodontally Accelerated Molar Distalization With Miniscrew Assisted Memory Screw: A Pilot Study

ST2 regulates bone loss in a site‐dependent and estrogen‐dependent manner

Cellular response within the periodontal ligament on application of orthodontic forces

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