Translation in regenerative medicine
Why promising regenerative results are unusually hard to move from laboratory to clinic.
Regenerative therapies translate poorly compared with conventional drugs, and the reasons are structural. A small molecule is a defined chemical with predictable behaviour. A cell-and-scaffold construct is a living, variable product whose potency depends on donor, culture history, and manufacturing — which makes consistency, not efficacy, the first obstacle.
Preclinical results also flatter. Rodent models heal far more readily than humans, so a scaffold that repairs a rat femur may do little in a human critical-size defect. Endpoints are harder too: radiographic bone formation is not the same as restored function, which is why surrogate endpoints deserve scrutiny.
None of this argues against the field — it argues for reading it carefully. Bench to bedside covers the pathway itself, and Clinical trial phases what each stage is actually designed to answer.
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- MethodsPreclinical modelsWhat animal models can and cannot tell you about human regeneration.
- MethodsClinical trial phasesWhat each stage of clinical testing is actually designed to answer.
- BoneCritical-size bone defectsThe threshold beyond which bone cannot bridge a gap on its own — and the problem most bone engineering exists to solve.
- FoundationsWhat is regenerative medicine?An introduction to the field that aims to restore the structure and function of damaged tissue rather than merely replace it.
- FoundationsThe principles of tissue engineeringCells, scaffolds, and signals — the three-part framework underlying most attempts to build living tissue.