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Role of Alveolar Bone Vasculature in...

Elzakra, Naseim,

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Role of Alveolar Bone Vasculature in Medication-Related Osteonecrosis of the Jaw (MRONJ) /

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Role of Alveolar Bone Vasculature in Medication-Related Osteonecrosis of the Jaw (MRONJ) // Naseim Elzakra.
作者:	Elzakra, Naseim,
面頁冊數:	1 electronic resource (100 pages)
附註:	Source: Dissertations Abstracts International, Volume: 86-12, Section: B.
Contained By:	Dissertations Abstracts International86-12B.
標題:	Dentistry. -
電子資源:	https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=32115829
ISBN:	9798280769649

Role of Alveolar Bone Vasculature in Medication-Related Osteonecrosis of the Jaw (MRONJ) /
Elzakra, Naseim,

Role of Alveolar Bone Vasculature in Medication-Related Osteonecrosis of the Jaw (MRONJ) /Naseim Elzakra. - 1 electronic resource (100 pages)

Source: Dissertations Abstracts International, Volume: 86-12, Section: B.

Background and HypothesisMedication-related osteonecrosis of the jaw (MRONJ) is a serious complication linked to antiresorptive medications used to treat bone malignancies, metastases, and osteoporosis. While its pathogenesis remains unclear, vascular insufficiency is considered a major contributing factor. Recent studies have identified transcortical canals (TCCs) in long bones that regulate vascular supply and undergo remodeling during inflammation. Preliminary data from our lab identified similar structures in the rat maxilla, termed alveolar bone cortical canals (ABCCs), suggesting a potential role in jawbone vascularization and MRONJ. We hypothesize that antiresorptive therapy disrupts ABCC remodeling, impairing vascularization and contributing to osteonecrosis.Materials and MethodsForty-eight female Sprague-Dawley rats were divided into saline- or zoledronic acid (ZA)- treated groups. Experimental periodontitis (EP) was induced via ligature placement. High-resolution micro-CT (1.8 µm voxel size) was used to assess ABCC architecture (density, volume, connectivity). DiI vessel painting and confocal imaging quantified vascular parameters. Histological assessments included H&E (bone integrity), TRAP (osteoclast activity), and immunohistochemistry (CD31, neutrophil elastase, F4/80). Osteocyte morphology and lacuno-canalicular networks were evaluated using phalloidin staining and Airyscan microscopy. Calcein double labeling assessed dynamic bone remodeling. An age-related microarchitecture study was conducted in male rats aged 4, 6, and 13 months.ResultsLow-resolution imaging confirmed MRONJ and EP. High-resolution imaging revealed ZA preserved cortical bone and prevented ABCC expansion in ligated sites. Vehicle-treated animals showed increased canal number and connectivity, indicating active vascular remodeling. ZA suppressed these changes and inhibited osteoclast-mediated turnover. Aging reduced canal connectivity and vascular perfusion. Phalloidin staining showed osteocyte alignment along cortical canals in vehicle-treated, ligated animals- suggesting a role in canal remodeling not seen in other groups.ConclusionThis study highlights the critical role of ABCCs in maintaining vascular integrity and bone remodeling in the context of MRONJ. Zoledronic acid treatment impaired osteoclast-mediated canal remodeling and reduced vascular perfusion. These changes may limit the bone's ability to respond to injury, contributing to osteonecrosis. The findings underscore the importance of intracortical vasculature in MRONJ pathogenesis, opening new directions for understanding how antiresorptive therapies affect bone healing and vascular dynamics in the jaw.

English

ISBN: 9798280769649Subjects--Topical Terms:

828971
Dentistry.
Subjects--Index Terms:

Osteoporosis

Role of Alveolar Bone Vasculature in Medication-Related Osteonecrosis of the Jaw (MRONJ) /
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520 $a Background and HypothesisMedication-related osteonecrosis of the jaw (MRONJ) is a serious complication linked to antiresorptive medications used to treat bone malignancies, metastases, and osteoporosis. While its pathogenesis remains unclear, vascular insufficiency is considered a major contributing factor. Recent studies have identified transcortical canals (TCCs) in long bones that regulate vascular supply and undergo remodeling during inflammation. Preliminary data from our lab identified similar structures in the rat maxilla, termed alveolar bone cortical canals (ABCCs), suggesting a potential role in jawbone vascularization and MRONJ. We hypothesize that antiresorptive therapy disrupts ABCC remodeling, impairing vascularization and contributing to osteonecrosis.Materials and MethodsForty-eight female Sprague-Dawley rats were divided into saline- or zoledronic acid (ZA)- treated groups. Experimental periodontitis (EP) was induced via ligature placement. High-resolution micro-CT (1.8 µm voxel size) was used to assess ABCC architecture (density, volume, connectivity). DiI vessel painting and confocal imaging quantified vascular parameters. Histological assessments included H&E (bone integrity), TRAP (osteoclast activity), and immunohistochemistry (CD31, neutrophil elastase, F4/80). Osteocyte morphology and lacuno-canalicular networks were evaluated using phalloidin staining and Airyscan microscopy. Calcein double labeling assessed dynamic bone remodeling. An age-related microarchitecture study was conducted in male rats aged 4, 6, and 13 months.ResultsLow-resolution imaging confirmed MRONJ and EP. High-resolution imaging revealed ZA preserved cortical bone and prevented ABCC expansion in ligated sites. Vehicle-treated animals showed increased canal number and connectivity, indicating active vascular remodeling. ZA suppressed these changes and inhibited osteoclast-mediated turnover. Aging reduced canal connectivity and vascular perfusion. Phalloidin staining showed osteocyte alignment along cortical canals in vehicle-treated, ligated animals- suggesting a role in canal remodeling not seen in other groups.ConclusionThis study highlights the critical role of ABCCs in maintaining vascular integrity and bone remodeling in the context of MRONJ. Zoledronic acid treatment impaired osteoclast-mediated canal remodeling and reduced vascular perfusion. These changes may limit the bone's ability to respond to injury, contributing to osteonecrosis. The findings underscore the importance of intracortical vasculature in MRONJ pathogenesis, opening new directions for understanding how antiresorptive therapies affect bone healing and vascular dynamics in the jaw.
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