The Hoof as the Sentinel of Systemic Failure: The Lameness Triad and the Susceptibility–Resilience Gate in Dairy Cows

Lameness is a major welfare and economic disorder in dairy production and a clinical sign with multiple causes. This review focuses on claw horn disruption lesions (CHDL), a major cause of periparturient lameness. Although hoof-centered prevention and treatment remain essential, preclinical systemic alterations, recurrence, and clustering with other transition-period disorders suggest that CHDL may sometimes represent the local expression of broader pathophysiology. We propose the Lameness Triad, in which three mechanisms converge: sustained endotoxemic pressure and TLR4-mediated innate immune activation, endothelial glycocalyx degradation and vascular dysfunction, and metabolic triage that reallocates resources from production toward defense. Their combined pathogenic pressure is proposed to produce clinical disease when it exceeds a cow-specific Susceptibility–Resilience Gate comprising mucosal barrier integrity, hepatic endotoxin clearance, immune calibration, redox reserve, hoof structural reserve, and prior damage. Ruminal dysbiosis, mammary involution, and postpartum uterine contamination may contribute to inflammatory and endotoxemic pressure, whereas the confined, continuously loaded digital corium may become a principal site of clinical expression. Longitudinal multi-omics studies identified inflammatory, urinary, and milk-metabolite alterations before diagnosis, with within-cohort serum and urine models discriminating cows that later became lame as early as eight weeks prepartum. These findings require prospective validation and do not establish the complete causal sequence. The framework extends, rather than replaces, established hoof-health programs and provides testable hypotheses for earlier detection, prevention, and selection for resilience.