Aging-related bone diseases are increasingly recognized as disorders in which uncoupled bone remodeling remains central but is substantially modified by immune-skeletal interactions. This review consolidates current evidence for osteoimmune senescence, a framework that links senescent skeletal cells, aging immune compartments, chronic SASP signaling, impaired immune clearance, and marrow-niche deterioration to reduced bone strength and repair. Osteoporosis, rheumatoid arthritis-associated erosion, osteoarthritis, periodontal bone loss, and delayed fracture healing are clinically distinct diseases, but they may share overlapping senescence-associated osteoimmune mechanisms while retaining disease-specific endotypes. Senescent osteocytes, osteoblast-lineage cells, and bone marrow stromal cells can increase RANKL/OPG imbalance, suppress osteogenesis, and reshape immune recruitment, whereas remodeled T cells, macrophages, neutrophils, and NK-cell surveillance pathways modify osteoclastogenesis and repair resolution. We also discuss gut-derived metabolites and imaging phenotypes as clinically important but non-specific readouts of this biology. DXA, HR-pQCT, MRI, CBCT, and molecular imaging cannot identify senescent cells directly, but they can anchor molecular hypotheses to tissue-level deterioration. Therapeutic translation will depend on matching senolytics, senomorphics, immune-recalibrating approaches, microbiota-derived metabolites, and bone-targeted delivery systems to disease stage, dominant cell population, and measurable skeletal endpoints.
