C H A P TE R 3

Inflammation and Healing1

Mark R. Ackermann

Key Readings Index

Acute Inflammation, 75
Substances Inducing the Acute
Inflammatory Response, 78
Fluidic (Exudative) Phase of the Acute
Inflammatory Response, 79
Endothelial Cell Dynamics during the
Acute Inflammatory Response, 79
Cellular Phase of the Acute Inflammatory
Response, 81
Leukocyte Adhesion Cascade, 81
Effector Cells of the Acute Inflammatory
Response, 83
Vascular Endothelial Cells, 83
Neutrophils, 84
Natural Killer Cells and Natural Killer T
Lymphocytes, 86
Monocytes and Macrophages, 86
Chemical Mediators of the Acute
Inflammatory Response, 87
Complement Cascade, 88
Cytokine Family, 93
Reparative Phase of the Acute
Inflammatory Response, 99
Nomenclature of the Inflammatory
Response (Morphologic
Diagnoses), 101
Morphologic Classification of
Exudates in Acute Inflammatory
Lesions, 102
Serous Inflammation, 102
Catarrhal Inflammation, 102
Fibrinous Inflammation, 103
Suppurative Inflammation, 104
Chronic Inflammation, 104
Progression of the Acute Inflammatory
Response to Chronic Inflammation,
Fibrosis, and Abscess Formation, 106
Healing by Fibrosis, 107
Abscess Formation, 107
Granulomatous Inflammation and
Granuloma Formation, 108
Gross and Microscopic Lesions and
Nomenclature of the Chronic
Inflammatory Response, 112
Cellular Mechanisms of Chronic
Inflammatory Responses, 113
Lymphocytes, 113
Monocytes/Macrophages, 113
Plasma Cells, 118
Wound Healing and Angiogenesis, 121

Injury or death of cells caused by infectious microbes, mechanical
trauma, heat, cold, radiation, or cancerous cells can initiate a well-
organized cascade of fluidic and cellular changes within living vas-
cularized tissue called acute inflammation (Fig. 3-1). These changes
result in the accumulation of fluid, electrolytes, and plasma proteins,
as well as leukocytes, in extravascular tissue and are recognized
clinically by redness, heat, swelling, pain, and loss of function of the
affected tissue. Inflammation is often a protective mechanism whose
biologic purpose is to dilute, isolate, and eliminate the cause of
injury and to repair tissue damage resulting from the injury. Without
inflammation, animals would not survive their daily interactions
with environmental microbes, foreign materials, and trauma and
with degenerate, senescent, and neoplastic cells.
Acute inflammation is the progressive reaction of vascularized
living tissue to injury over time. This process is usually a well-
ordered cascade mediated by chemoattractants, vasoactive mole-
cules, proinflammatory and antiinflammatory cytokines and their
receptors, and antimicrobial or cytotoxic molecules. Acute inflam-
mation has a short duration, ranging from a few hours to a few days,
and its main characteristics are exudation of electrolytes, fluid, and
plasma proteins and leukocytic emigration, principally neutrophils
1 Information on this topic, including E-Table 3-1, is available at
For a glossary of abbreviations and terms used in this chapter see
E-Glossary 3-1.
from the microvasculature, followed by rapid repair and healing. For
convenience, acute inflammation is divided into three sequential
phases: fluidic, cellular, and reparative.
Chronic inflammation is considered to be inflammation of pro-
longed duration, usually weeks to months and even years, in which
the response is characterized predominantly by lymphocytes and
macrophages, tissue necrosis, and accompanied by tissue repair, such
as healing, fibrosis, and granulation tissue formation, all of which
may occur simultaneously. Chronic inflammation can be a sequela
to acute inflammation if there is failure to eliminate the agent or
substance that incites the process. With such persistent substances
the inflammatory reaction and exudates gradually transition from
seroproteinaceous fluids and neutrophils to macrophages, lympho-
cytes, and fibroblasts with the potential for formation of granulomas.
Alternatively, some inciting substances can invoke chronic inflam-
mation directly and almost immediately. Examples include infec-
tions by Mycobacterium spp.; exposure to foreign materials, such as
silicates and grass awns; and immune-mediated diseases, such as
arthritis.
Evolution of the Current Understanding
of Inflammation
www.expertconsult.com.

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