Glucocorticoid therapy for myasthenia gravis resulting in resorption of the mandibular condyles

Cowan, Jay; Moenning, John E.; Bussard, David A.

doi:10.1016/0278-2391(95)90130-2

Cited by 8 publications

(1 citation statement)

References 5 publications

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“…However, the extent to which PLR in the mandible is sensitive to glucocorticoids has yet to be studied. Osteonecrosis of mandibular bone occurs in patients with autoimmune diseases, such as vasculitis, who are being treated with high dose steroids ( Cowan et al, 1995 ). Although the extent to which glucocorticoids are responsible for this pathology is unclear, an understanding of the role of PLR in the mandible could improve strategies to prevent and treat osteonecrosis, particularly in this high risk population ( Strojan et al, 2017 ; Chronopoulos et al, 2018 ).…”

Section: Introductionmentioning

confidence: 99%

Glucocorticoids cause mandibular bone fragility and suppress osteocyte perilacunar-canalicular remodeling

et al. 2018

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Osteocytes support dynamic, cell-intrinsic resorption and deposition of bone matrix through a process called perilacunar/canalicular remodeling (PLR). In long bones, PLR depends on MMP13 and is tightly regulated by PTH, sclerostin, TGFβ, and glucocorticoids. However, PLR is regulated differently in the cochlea, suggesting a mechanism that is anatomically distinct. Unlike long bones, the mandible derives from neural crest and exhibits unique susceptibility to medication and radiation induced osteonecrosis. Therefore, we sought to determine if PLR in the mandible is suppressed by glucocorticoids, as it is in long bone. Hemimandibles were collected from mice subcutaneously implanted with prednisolone or vehicle containing pellets for 7, 21, or 55 days (n = 8/group) for radiographic and histological analyses. Within 21 days, micro-computed tomography revealed a glucocorticoid-dependent reduction in bone volume/total volume and trabecular thickness and a significant decrease in bone mineral density after 55 days. Within 7 days, glucocorticoids strongly and persistently repressed osteocytic expression of the key PLR enzyme MMP13 in both trabecular and cortical bone of the mandible. Cathepsin K expression was significantly reduced only after 55 days of glucocorticoid treatment, at which point histological analysis revealed a glucocorticoid-dependent reduction in the lacunocanalicular surface area. In addition to reducing bone mass and suppressing PLR, glucocorticoids also reduced the stiffness of mandibular bone in flexural tests. Thus, osteocyte PLR in the neural crest-derived mandible is susceptible to glucocorticoids, just as it is in the mesodermally-derived femur, highlighting the need to further study PLR as a target of drugs, and radiation in mandibular osteonecrosis.

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Section: Introductionmentioning

confidence: 99%

Glucocorticoids cause mandibular bone fragility and suppress osteocyte perilacunar-canalicular remodeling

et al. 2018

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Nonsurgical Management of Temporomandibular Disorders

Karlis

Glickman

2022

Peterson’s Principles of Oral and Maxillofacial Surgery

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Steroid induced osteonecrosis: An analysis of steroid dosing risk

Powell

Chang²,

Naguwa

et al. 2010

Autoimmunity Reviews

145

149

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Osteonecrosis is a serious condition involving bone destruction that frequently requires surgical treatment to rebuild the joint. While there is an abundance of literature documenting corticosteroid related osteonecrosis, there is no consensus as to the relative risk of osteonecrosis after administration of steroids via parenteral, oral, topical, inhaled and other routes. This risk is an important prognostic indicator because identification and conservative intervention can potentially reduce morbidity associated with aggressive surgical treatment of osteonecrosis. This paper provides insight into establishing guidelines related to the risk of developing osteonecrosis as a result of corticosteroid use. Case studies, retrospective studies and prospective studies in humans on different corticosteroids and varied dosages were assessed. Most cases of osteonecrosis are secondary to systemically administered corticosteroids and/or high dose daily therapy, particularly in patients with underlying comorbidities including connective tissue diseases, hyperlipidemia, or previous trauma. Previous case reports of osteonecrosis related to inhaled or topical use of steroids are complicated by the fact that in the great majority of cases, the patients are also treated with systemic steroids prior to the development of osteonecrosis. Based on the literature, a set of recommendations regarding the risk of osteonecrosis in patients on steroids was formulated.

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Glucocorticoid therapy for myasthenia gravis resulting in resorption of the mandibular condyles

Cited by 8 publications

References 5 publications

Glucocorticoids cause mandibular bone fragility and suppress osteocyte perilacunar-canalicular remodeling

Glucocorticoids cause mandibular bone fragility and suppress osteocyte perilacunar-canalicular remodeling

Nonsurgical Management of Temporomandibular Disorders

Steroid induced osteonecrosis: An analysis of steroid dosing risk

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