Acute inflammation occurs immediately after an injury and is usually short-lived, lasting hours to a few days.

Chronic inflammation is an unhealthy inflammatory over-response that can linger for months to years. Many diseases have been linked to chronic inflammation. ACUTE INFLAMMATION
PULSE OF INJURY ONSET IS ABRUPT, WELL-DEFINED PROMINENT SYMPTOMS PROMINENT VASCULAR EFFECTS AND EXUDATE

CHRONIC INFLAMMATION
PERSISTENT INJURY VAGUE ONSET SYMPTOMS ARE OFTEN SUBDUED, AND/OR INSIDIOUS MILD TISSUE EFFECTS EXUDATE IS MADE OF

EXUDATE IS NEUTROPHILS

BOTH LYMPHOCYTES

AND MACROPHAGES

CT PROLIFERATION OCCURS AFTER CT PROLIFERATION IS CONCURRENT WITH INFLAMMATION SUBSIDES ON-GOING INFLAMMATION

MEDIATORS IN ACUTE INFLAMMATION - HISTAMINE (CELL-DERIVED/PREFORMED GRANULES)- EARLY VASODILATION AND PERMEABILITY - PG (CELL-DERIVED - MAST CELLS AND

LEUKOCYTES)- CAUSES VASODILATION, PERMEABILITY, PAIN, AS WELL AS POTENTIATES OTHER MEDIATORS - LT (CELL-DERIVED)- CHEMOTAXIN TO NEUTROPHILS AND INCREASES VASCULAR PERMEABILITY - N.O.- VASODILATION AND HELPS WITH MACROPHAGES ANTIMICROBIAL ABILITY - BRADYKININ- PLASMA DERIVED FACTOR INVOLVED WITH ACITIVATION OF CLOTTING FACTORS AND IS IMPORTANT WITH RESPECT TO VASODILATION/PERMEABILITY AND PAIN - C3A- VASOLDILATION AND PERMEABILITY - C3B-OPSONIN - C5A- VASOLDILATION, PERMEABILITY AND CHEMOKINE - PAF- PLATELET ACITIVATION, VASODILATION AND PERMEABILITY - TNF-ALPHA- ACITVATES MACROPHAGES - IL-1- ACTIVATE MACROPHAGES AND FEVER - IL-8- CHEMOTAXIN FOR POLYS - FIBRINOPEPTIDES- PERMEABILTIY AND CHEMOTAXIN - FIBRINOLYTICS- AVTIVATES FACTOR XII AND COMPLEMENT COMPONENTS C3A AND C5A

MEDIATORS IN CHRONIC INFLAMMATION - ALONG WITH THE AFOREMENTIONED MEDIATORS N ACUTE INFLAMMATION, THERE IS ALSO AN INCREASED CYTOKINE PRODUCTION OF TNF-ALPHA. - THE T-CELLS ALSO PRODUCE INF-GAMMA, WHICH IS THE MOST POWERFUL ACTIVATOR OF MACROPHAGES Read more: http://wiki.answers.com/Q/Difference_betw een_acute_and_chronic_inflammation#ixzz1Y7cSrJ Fn