In a mouse model carrying two coexisting mitochondrial genomes (heteroplasmy), osteoclast precursors showed reduced incorporation of respiratory complex I subunits into mitochondria, impaired ATP production, exhausted autophagic flux and blocked differentiation into bone-resorbing cells. The autophagy inducer spermidine restored mitochondrial health and osteoclast activity in these mice and in cells from patients with primary mitochondrial disease. The evidence comes from mice and patient-derived cells, not from human treatment. Mitochondrial disease patients often suffer poor bone health, and this work offers a mechanistic explanation: faulty energy supply stalls the cells that remodel bone. Spermidine is already a popular longevity supplement, but the finding applies to a narrow situation, inherited mtDNA mutations, and does not show that supplementing spermidine protects bone in healthy adults or ordinary osteoporosis. Doses in mice may not translate to dietary or supplement intake, and rescue in patient cells in a dish is far from a clinical outcome. No human trial has tested spermidine for bone health. This is a preprint awaiting peer review, so the conclusions may change. Editorially, the work is incremental but useful: it extends spermidine's autophagy-based benefits to a new tissue and clarifies why mitochondrial dysfunction disrupts skeletal maintenance, a link also relevant to age-related bone loss.