GRANULOMATOUS INFLAMMATION
(Tuberculosis vs. Sarcoidosis)
Objectives: To define: 1) the hallmarks of
cells and events of granulomatous inflammation; 2) the mechanisms of foreign body and
immunologic granulomas; 3) compare and contrast the features and mechanisms of
granolomatous inflammation seen in tuberculosis vs. sarcoidosis; and 4) the outcomes of
granulomatous inflammation.
SUMMARY
When acute inflammatory processes are unable to resolve the trauma this often leads to
a sustained or continuing inflammatory reaction known as chronic inflammation. Generally,
chronic inflammation can be histologically divided into two broad categories: diffuse
chronic inflammation and granulomatous inflammation. Both of forms of chronic inflammation
are histologically characterized by the appearance of infiltration of mononuclear cells
including macrophages, lymphocytes and plasma cells. Additionally, chronic inflammation is
often associated with the proliferation of fibroblasts as well as increased present of
connective tissue or fibrosis. In a diffuse chronic inflammation, the distribution of
mononuclear cells is generally even throughout the involved tissue. In contrast,
granulomatous inflammation is characterized by a distinct pattern of small granular
appearing accumulation of epitheloid macrophages ringed by lymphocytes, known as
granulomas. A second key histologic feature of these granulomas is the presence of
Langhans or giant cells. These giant cells represent the coalescence or fusion of multiple
macrophages, and are characterized by being multinucleated. The etiologic agents
responsible for chronic inflammation may range from infectious agents to indigestible
particles, as well as a role for immunologic factors which are involved in cell-mediated
immunity. Regardless of the underlying agent or cause of chronic inflammation, often
tissue destruction is a major feature of chronic inflammation. This tissue destruction may
take the form of total loss of tissue architecture and function as occurs in cavitation in
the lungs of tuberculosis patients.
In summary, inflammation represents a complex group of vascular and cellular events which are generally under the control of a variety of chemical signals known as inflammatory mediators. These mediators control the movement of fluid and cells into tissue, as well as the activation of these leukocytes in the tissue. If the insighting agent is removed by acute inflammation, the formation of granulation tissue and healing proceeds. Alternatively, if acute inflammation does not resolve the trauma, it often leads to chronic inflammation and the ultimate destruction of the tissue. Thus, inflammation remains at two-edge swords that can both protect and destroy with equal swiftness and effectiveness.
LECTURE OUTLINE
I. Purpose, Definition and Causes
II. Hallmarks of Chronic Inflammation
A. Time
B. Cells (mononuclear)
III. Cells
A. Macrophage
B. Lymphocytes
C. Epitheliod cells
D. Giant cells
IV. Granulomas
A. Foreign body
B. Immunologic
VI. Foreign Body Reactions
A. Features and mechanisms
VII. Immunologic Reaction
A. Features and mechanisms
VIII. Definition of Granulomatous Inflammation
IX. Tuberculosis
A. Etiology: mycobacteria
B. Pathology
C. Pathogenesis
1. Virulence of organism
2. Immune status
3. Tissue destruction
D. Primary Tuberculosis
E. Secondary or disseminated tuberculosis
F. Outcome
X. Sarcoidosis
A. Etiology: unknown
B. Pathology
C. Pathogenesis
1. Role of microorganisms
2. Role of immune system
D. Outcome
Required Reading: Pathological Basis of Disease, Robbins et al., pp.
324-327 and 712-714.
Study Questions: