Infiltration by lymphocytes demonstrates immune response in tissue
May develop after acute inflammation or may be a primary response to certain stimuli
Predisposing factors include persistent damaging stimulus, inadequate host response to infection and persistent autoimmune disease
necrotic cell debris, acute inflammatory exudate, vascular and fibrous granulation tissue, lymphoid cells, macrophages and collagenous scar
1) defective inflammation- chronic inflammatory response cannot be elicited, causing increased susceptibility, delayed wound healing, and tissue damage
2) excess inflammation- seen in allergies, plays a role Cancer, Atherosclerosis, Autoimmune disease
Fibrosis as a sequel of chronic infections, metabolic conditions
Unchecked substances that lead to tissue injury
Cause excess inflammation
Toxic O2 metabolites
Neutrophil chemotactic factors
Unchecked substances that lead to Fibrosis
(PDGF, FGF, TGG-b)
Angiogenesis factors (FGF)
Chronic inflammation diseases
Chronic peptic ulcer
infections with persistent microbes
autoimmune disorders (RA, SLE)
prolonged exposure to toxic agents
(foreign body reactions)
Chronic Peptic Ulcer
Protective mechanism of upper alimentary track breaks down
HCL and proteolytic enzymes destroy epithelium and supporting stroma Acute inflammatory reaction
Acute inflammatory reaction occurs
-formation of exudate close to the acid exposed surfaces while in the depths of the ulcer (farthest from the acid) attempts are made to organize the exudate and granulation tissue forms Collagenous scar
Ulceration of the wall stomach or duodenum persistent damage
local defect, or excavation, of the surface of an organ or tissue that is produced by the sloughing(shedding) of inflammatory necrotic tissue
Cellular attempt to contain an offending agent that is difficult to eradicate.
In this attempt there is often strong activation of T lymphocytes leading to macrophage activation, which can cause injury to normal tissues.
Distinctive pattern of chronic inflammation that is encountered in a limited number of infectious and some noninfectious conditions.
Recognition important in the clinic: limited number of possible conditions that cause it and the significance of the diagnoses associated with the lesions
discrete clusters of macrophages and lymphocytes
Macrophages develop an epithelial-like (epithelioid) appearance (GRANULOMA)
In time develops an enclosing rim of fibroblasts and connective tissue (Fibrosis)
Caused by insoluble particles that are capable of inducing a cell-mediated immune response
Macrophages are transformed into Epitheloid cells and multinucleate giant cells
Tuberculosis *** (high incidence due to drug resistant stains)
Schistosomiasis (3 types)
2.Foreign Body Granulomas
Don’t incite either an inflammatory or immune response.
Epitheloid cells and giant cells are apposed to the surface and encompass the foreign body.
The foreign body is usually found in the center of the granuloma.
Bad systemic disease, probably autoimmune disease
Etiologic agent is unknown
Granuloma histological example
Caseous necrosis at center
Macrophages and epithelioid cells
Lymphocytes & plasma cells- form a ring
Central necrosis surrounded by a collection of large, activated macrophages that have some resemblance to epithelial cells; “epithelioid” cells
Langhan's giant cells
Outside and around the macrophages is a collar border of lymphocytes
Over time, some fibroblasts appear in the lymphocytic collar (macrophage cytokine recruitment)
Langhan’s giant cells
activated macrophages that fuse to form large, multinucleated cells.
Many nuclei around the periphery and a large central cytoplamic mass