Chronic Inflammation Flashcards
(26 cards)
What’s Chronic Inflammation?
Inflammation of prolonged duration in which active inflammation, tissue destruction and attempts at repair are proceeding simultaneously
What are the predominant cell types in chronic inflammation?
- Lymphocytes
- Plasma cells
- Macrophages
Does chronic inflammation always proceed acute inflammation?
No
- May follow acute inflammation which it does not resolve but it can begin insidiously
What are the 3 causes of primary chronic inflammation?
- Resistance of infective agent to phagocytosis
- Endogenous materials
- Necrotic adipose tissue, bone, uric acid, keratin (epithelial/’sebaceous’ cyst), hair (pilar cysts) - Exogenous materials
- Silica (dust + pulmonary lung fibrosis), suture material (foreign nature of material can illicit an immune response), prosthesis, splinter - Autoimmune diseases
- Lichen planus (oral)
- Non-organic specific e.g. Rheumatoid arthritis
- Contact hypersensitivity - Specific diseases of unknown aetiology
- Chronic inflammatory bowel disease e.g. ulcerated colitis
- Primary granulomatous diseases e.g. Crohn’s disease
- Progression from acute inflammation
- Osteomyelitis
- *Recurrent episodes of acute inflammation
- Chronic cholecystitis
What are the effects of Chronic inflammation?
- Infiltration with mononuclear cells
- Macrophages etc - Tissue destruction
- Attempts at healing
What’s an ulcer?
A loss of an epithelial lining so the underlying tissue is exposed - granulation tissue is produced and that’s why it can appear raised
What’s the microscopic appearance in acute inflammation?
- Cellular infiltrate
- Multinucleate giant cells
- Production of new fibrous tissue
- Continuing destruction
Is chronic inflammation a self perpetuating cycle of destruction?
Yes
What’s the dominant immune cell in chronic inflammation?
Macrophages
- Circulate as monocytes
- Emigrate into the extravascular tissue early in acute inflammation
- Macrophage activation is mediated by cytokines (IFN-gamma, endotoxins and chemical mediators)
- Activation leads to an increase in cell size, lysosomal enzymes, more active metabolism and greater phagocytosis
HOWEVER
- Biological active produces secreted by macrophages lead to tissue injury and fibrosis (i.e. chronic inflammation)
What biological produces of activated macrophages cause 1. tissue injury and 2. fibrosis
1.
- Proteases
- Coagulation factors
- AA metabolites
- Nitric Oxide
2.
- Growth factors (PDGF, TGFbeta)
- Fibrogenic cytokines
- Remodelling collagenesis
What are the other cells in chronic inflammation?
- Lymphocytes
- T cells = produce cytokines to attract, hold and activate macrophages
- B cells = antibody production - activate macrophages via secretion of TNF, IL-1 and chemokines – persistent in inflammatory response - Plasma cells = differentiated B cell which produce antibodies
- Eosinophils = Mediated by Immunoglobulin E and parasitic infections
- release TGF, VEGF, PDGF - Mast cells = widely distributed and release histamine and products of arachidonic acid oxidation (prostaglandins=inflammation)
- Neutrophils = particularly if persisting microbes
- type of phagocyte
What’s necrotic tissue?
Tissue which is undergoing unplanned cell death - stimulated by chronic inflammation and this then stimulates necrosis - positive feedback cycle
- perpetuates inflammatory cascade by the activation of:
1. Kinin (vasodilation)
2. Coagulation
3. Complement
4. Fibrinolytic system
5. Mediators released from leukocytes
6. Uric acid released from dying cells
What’s Granulomatous inflammation?
- Distinctive pattern of chronic inflammation
- Characterised by focal accumulation of activated amcrophges which often develop epithelial-like patterns (look like epithelial cells)
- Immunologically mediated, infectious and non0infectious conditions
What are the characteristics of Granulomas?
- Large vesicular nuclei, folded nuclear membrane, plentiful eosinophilic granular cytoplasm and indistinct cell borders
- Hypoxic centre
- Little phagocytic activity and more secretory function
- Can contain giant cells and surrounded by lymphocytes
- Typically, the offending pathogen will be at the centre of the granuloma
What are Giant cells?
- Accumulated of macrophages
- Form when foreign particles are too large to be ingested by just 1 macrophage - fuse together
- Large cytoplasm with multiple nuclei
- Not always granuloma for giant cells to be present
What are Langhans’ giant cells?
Typically found in TB patients
- The peripheral rim of nuclei
- Large eosinophilic cytoplasm
What are Immune granulomas?
- Insoluble particles such as microbes induce cell mediated immune responses
- Macrophages engulf material, process and present it to T-Helper cells
- T-Helper cells produce IL-2 which activates other T-cells and INF-gamma which activates macrophages = multinucleate giant cells
Give some examples of non-infective granulomas
- Rheumatoid disease - systemic
- Crohn’s disease - can present orally with inflammation of lips/tongue/cheeks
- Dentists can be the 1st to identify Crohn’s
What’s Pyogenic Granulomata?
Technically it should be called Lobular Capillary Haemangioma - growth of blood vessels (capillaries)
- Not granulomatous
- Not purulent
- Caused by irritation, trauma, hormones and poor hygiene - harmless swelling
- Bleeds readily due to being made of blood vessels
- CAN BE CAUSED BY A DENTURE
What are the 3 factors in Chronic inflammation healing and repair?
- Organisation: of specialised tissue
- Formation of granulation tissue
- Wound healing
What happens during the organisation in chronic inflammation healing and repair?
- Dead tissue is removed by phagocytosis via macrophages/phagocytes
What’s granulation tissue?
Collection of fibroblasts and collagen deposits, macrophages
- Agiogenesis occurs
What are the products of granulation tissue?
Fibrous tissue (scar) - small firm blemish on skin
What are the problems associated with granulation tissue?
Peritonitis (inflammation of lining of stomach)
- adhesion between loops of bowel following Peritonitis cna prevent the bowl from contracting properly
- Unsightly scar formation
- When granulation tissue replaces heart muscle it cannot contract so it impairs heart function
