Slipping rib syndrome (SRS) is an underrecognized cause of lower anterior chest wall pain resulting from hypermobility of the 8th-10th costal cartilages. Because the condition represents a dynamic instability, conventional imaging is often normal, and the diagnosis is primarily clinical. A 45-year-old woman presented with sharp pain localized to the right 8th-10th costal margin, aggravated by trunk movements. Laboratory and radiologic evaluations were unremarkable, and hepatobiliary causes were excluded. The patient did not respond to oral or topical non-steroidal anti-inflammatory drugs or conventional physical therapy. At follow-up, the hooking maneuver reproduced the pain and demonstrated anterior rib displacement, confirming the clinical diagnosis of SRS. Kinesiotaping was applied to provide mechanical stabilization of the affected rib segment. The patient experienced a rapid reduction in pain, with the VAS score decreasing from 8 to 3 within one week and complete symptom resolution by the third week. A recurrence one year later responded successfully to the same stabilization protocol. This case highlights the diagnostic challenges of imaging-negative SRS and suggests that targeted mechanical stabilization using kinesiotaping may be an effective, reproducible, non-invasive, conservative treatment option prior to invasive interventions.
Osteocytes, long considered passive residents of bone, are now recognized as master regulators of skeletal remodeling and systemic metabolism. This review synthesizes current knowledge on osteocyte signaling, evaluates mechanotransduction mechanisms, and identifies key knowledge gaps to guide future research. A narrative review was conducted using MEDLINE, PubMed, Embase, Cochrane CENTRAL, and Google Scholar for studies published between January 2016 and December 2024. Keywords included “osteocyte signaling,” “bone homeostasis,” and “mechanotransduction.” Included studies encompassed experimental, preclinical, translational, and clinical research. Osteocytes coordinate bone formation and resorption through paracrine and endocrine mediators, including sclerostin, receptor activator of nuclear factor-κB ligand, wingless-related integration site ligands, and fibroblast growth factor 23. Their extensive lacuno-canalicular network facilitates mechanosensation via fluid shear stress, ion channels (e.g., Piezo1), and cytoskeletal remodeling. Osteocytes also influence mineral metabolism, immune responses, energy homeostasis, and aging. Emerging evidence highlights their heterogeneity and context-dependent signaling, though debates persist regarding primary mechanosensors, signal hierarchy, and spatial regulation of outputs. Osteocytes act as central integrators of mechanical and biochemical cues, orchestrating skeletal and systemic physiology. Advancing in vivo models, spatial transcriptomics, and mechanistic studies will deepen understanding of osteocyte signaling, offering promising therapeutic avenues for osteoporosis, metabolic bone disorders, and chronic inflammation.
