Osteocytes, the most abundant cells in bone, are altered in Paget's disease lesions, displaying increased size, decreased canalicular length, incomplete differentiation, and less sclerostin expression compared to controls in both patients and mouse models. Pagetic lesions show increased senescent osteocytes that express RANK ligand, which drives osteoclastic bone resorption. Abnormal osteoclasts in Paget's disease secrete abundant IGF1, which enhances osteocyte senescence, contributing to lesion formation. Recent data suggest that osteocytes contribute to lesion formation in Paget's disease by responding to high local IGF1 released from abnormal osteoclasts. Here we describe the characteristics of osteocytes in Paget's disease and their role in bone lesion formation based on recent results with mouse models and supported by patient data.
Keyphrases
- bone loss
- bone mineral density
- end stage renal disease
- poor prognosis
- soft tissue
- chronic kidney disease
- ejection fraction
- electronic health record
- binding protein
- machine learning
- postmenopausal women
- newly diagnosed
- dna damage
- prognostic factors
- pi k akt
- big data
- patient reported outcomes
- long non coding rna
- cell proliferation
- peritoneal dialysis
- deep learning
- data analysis