This episode explains bone scans as functional, nuclear medicine tests that reveal bone metabolism—blood flow, inflammation, infection, and repair—often before structural imaging shows changes.

Learn the three phases (flow, blood pool, delayed), how osteomyelitis typically lights up all phases, pitfalls like Charcot foot and ischemia, and advanced options (SPECT‑CT, labeled white blood cell scans, PET) that improve diagnosis and guide limb‑salvage decisions.

In this episode we break down skin substitutes for diabetic foot ulcers: how they work biologically, why they are not interchangeable, and common errors clinicians make.

We review major categories and examples (bioengineered cellular grafts like Apligraf and Dermagraft; human dermal matrices like AlloDerm and GraftJacket; placental/amniotic products like EpiFix and Grafix; xenografts such as Integra; and synthetic matrices like OASIS), plus inclusion/exclusion criteria.

Practical application rules are emphasized: sharp debridement to bleeding tissue, infection control, optimized perfusion, strict offloading, proper dressing, and documentation. Stop after 2–3 failed applications and remember grafts are tools—not cures.

This episode explains that diabetic foot ulcers are driven by "biological paralysis" rather than just skin loss, describing the four phases of wound healing and why wounds get stuck in chronic inflammation.

Dr. G reviews key failure mechanisms—protease imbalance, fibroblast dysfunction, persistent M1 macrophages, angiogenic failure, and stem cell impairment—and how skin substitutes can replace extracellular matrix, rebalance cytokines, provide growth-factor signaling, and support tissue repair.

The episode also covers when skin substitutes fail (infection, ischemia, inadequate debridement, and mechanical disruption) and emphasizes matching the graft to the wound biology rather than just wound size.