A patient with a significant laceration takes high-dose NSAIDs (prostaglandin synthesis inhibitors) continuously throughout the healing period. What is the most likely consequence?
AFaster healing, because reducing inflammation prevents tissue damage from immune cells
BNo significant effect, because NSAIDs only affect fever and systemic pain
CImpaired healing, because prostaglandins and the inflammatory response are required to recruit the cells that drive repair
DFaster initial healing but permanent impairment of the final remodeling phase
Inflammation is not incidental to wound healing — it triggers the entire repair sequence. Prostaglandins contribute to vasodilation and vascular permeability that deliver immune cells to the wound. Macrophages recruited during inflammation release growth factors that signal the transition to the proliferative phase. Suppressing inflammation aggressively can delay neutrophil and macrophage recruitment, stall the proliferative phase, and ultimately slow healing. Option A is the dangerous misconception that inflammation is purely harmful.
Question 2 Multiple Choice
Three days after a skin laceration, which cell type should be most dominant at the injury site?
APlatelets, which continue forming the clot for days after injury
BNeutrophils, the primary immune cells throughout the entire healing response
CMacrophages, which have replaced the initial neutrophil infiltrate
DFibroblasts, which begin laying down collagen immediately after injury
Wound healing follows a strict temporal sequence. Neutrophils arrive first (within hours) and dominate for 24–48 hours, clearing bacteria and debris. By day 2–3, neutrophil numbers decline and macrophages take over. Macrophages persist longer, continue phagocytosis, and critically, release growth factors that initiate the proliferative phase. Platelets are relevant only in the hemostasis phase (minutes to hours). Fibroblasts don't arrive until the proliferative phase, which begins several days after injury.
Question 3 True / False
Scar tissue, even after the full remodeling phase is complete, has reduced tensile strength compared to the original unwounded skin, typically reaching only about 80% of normal.
TTrue
FFalse
Answer: True
Despite months of remodeling in which disorganized collagen is broken down and replaced, scar tissue never fully recapitulates the original dermal architecture. Original dermis has a basket-weave pattern of collagen fibers running in multiple directions, distributing mechanical stress efficiently. Scar tissue has parallel-oriented collagen bundles that are weaker under multidirectional stress. Scars also lack hair follicles and sweat glands. The ~80% tensile strength reflects this permanent architectural difference.
Question 4 True / False
Inflammation is a pathological response to injury that delays healing and should be suppressed as quickly as possible to promote recovery.
TTrue
FFalse
Answer: False
This is a common and consequential misconception. Inflammation is a carefully regulated protective response essential for healing. It delivers neutrophils to kill pathogens, recruits macrophages that bridge the transition to the proliferative phase, and establishes the vascular permeability needed for immune and repair cells to reach the wound. Suppressing inflammation too aggressively — as with high-dose corticosteroids — impairs pathogen clearance, delays macrophage-driven signaling, and can stall healing entirely. The goal is resolution of inflammation, not its elimination.
Question 5 Short Answer
Why are macrophages described as the critical bridge between the inflammatory and proliferative phases of wound healing? What would happen if macrophages were absent?
Think about your answer, then reveal below.
Model answer: Macrophages perform two essential bridging functions: they complete the clean-up begun by neutrophils (phagocytosing debris and dead neutrophils), and they secrete growth factors — including VEGF, PDGF, and TGF-β — that signal fibroblasts and endothelial cells to begin the proliferative phase. Without macrophages, the wound cannot transition from destruction to rebuilding. Experimental depletion of macrophages results in wounds stuck in the inflammatory phase, with impaired granulation tissue formation, reduced angiogenesis, and severely delayed closure.
The macrophage's dual role is the key insight: it is both a continuation of the innate immune response (phagocytosis) and the initiator of the repair program (growth factor release). Macrophages evolve through functional states during healing — early inflammatory (M1-like) macrophages clear debris, while later repair (M2-like) macrophages promote tissue remodeling. Disturbances to this transition (as in chronic wounds or diabetic ulcers) result in macrophages stuck in the inflammatory state unable to initiate repair.