Inflammatory Phase

The inflammatory phase follows haemostasis and occupies roughly the first four to six days of an uncomplicated wound. Chemokines from platelets and activated complement draw neutrophils in within hours to clear bacteria and necrotic debris. Monocytes follow and become macrophages, which clear apoptotic neutrophils and then shift phenotype, from a pro-inflammatory profile rich in TNF-alpha and IL-1 to a reparative one secreting TGF-beta and VEGF. That shift is what licenses the proliferative phase.

The phase is not simply destructive. Depleting macrophages in mouse wound models delays closure and impairs angiogenesis rather than helping. In bone, cyclooxygenase inhibition retards union in rodent fracture models, and prostaglandin signalling is needed for normal callus formation. Human data on anti-inflammatory drugs and fracture or tendon healing are observational and confounded by why the drug was taken; the question is unsettled, not answered.

That makes suppression a tradeoff, not a free improvement: blunting the phase reduces pain and swelling while also removing the debridement and the growth-factor burst the next phase depends on. What matters clinically is usually resolution rather than magnitude, since healing tissue switches inflammation off on schedule, whereas a chronic wound sits in a stalled inflammatory state for months with high protease activity.

The recurring error is treating anti-inflammatory action as synonymous with pro-healing action. Recovery peptides are routinely supported by a cytokine reduction in cell culture and then described as accelerating repair, an inference the data do not carry. The related misuse is the injury-timing protocol built on an inflammatory window borrowed from rodent work, where the timetable is compressed and species-specific.