CHRONIC INFLAMMATION

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1 CHRONIC INFLAMMATION Chronic inflammation is an inflammatory response of prolonged duration often for months, years or even indefinitely. Its prolonged course is proved by persistence of the causative agent in the tissues. Often the persistent inflammatory changes are combined with attempts at healing. Factors influencing the chronic inflammatory response: 1. The nature of the damaging agent. 2. The resistance of the host. The balance between these two factors determines the course of the response and its final outcome. Nature of the Damaging Agent 1. Non-living agents Exogenous: Physical eg X-rays Chemical a) liquids eg liquid phenol b) solids eg particulate silica c) gases eg cadmium fumes Endogenous: Keratin Hair 2. Living agents (micro-organisms) Bacteria eg Mycobacterium tuberculosis Mycobacterium leprae Spirochaete eg Treponema pallidum Fungi eg Actinomycosis bovis Cryptococcus neoformans. 3. Cause Unknown Micro-organisms which produce chronic inflammation differ from those which cause acute inflammation in the following ways. 1. They are not successfully phagocytosed by polymorphs. 2. They can survive and multiply in the cytoplasm of macrophages. 3. They do not produce toxins. The Resistance or Immunity of the Host: The resistance or immunity of the host is the ability to withstand the disease producing properties of the chronic inflammatory agent. The immunological mechanisms involved are similar overall to those utilised in acute inflammation but

2 cellular immunity plays a more prominent role in chronic inflammation and the role of humoral antibodies is less important. Delayed hypersensitivity mediated by specifically primed T-lymphocytes produced in the cell mediated immune response plays a major and fundamental role in many chronic inflammatory diseases. Other host factors influencing healing or progression are impaired nutrition and blood supply and endocrine factors. Histological features of chronic inflammatory response: 1. Cells involved in the chronic inflammatory response: Macrophage, which can become epithelioid cells and giant cells Lymphocyte and Plasma cell. 2. General Features a) Necrosis Necrosis is due to cell death in the centre of the lesion caused by the action of micro-organisms, endarteritis and in some cases delayed hypersensitivity. b) Attempts at healing These consist of proliferation of endothelial cell to form blood and lymphatic channels, proliferation of fibroblasts and collagen formation and accumulation of lymphocytes and plasma cells. Granulation formation: A granuloma is a microscopic, focal, chronic inflammatory lesion composed of macrophages, sometimes with other cells as well, such as giant cells. Examples of Granulomatous Inflammation: Tuberculosis Leprosy Sarcoidosis Granulomatous Inflammation: 1) Is seldom entirely specific histologically 2) Is often associated with hypersensitivity Chronic Inflammation of Unknown Cause: eg Crohn s disease Rheumatoid arthritis Sarcoidosis All are chronic diseases persisting for many years and the histological features seen conform with the general histological features of chronic inflammation. Effects of final Healing after Chronic Inflammation:

3 1. Replacement of functioning tissue by fibrous tissue eg lung in silicosis. 2. Adhesions in serosal cavities eg constrictive pericarditis 3. Stricture formation eg in Crohn s disease. Examples of chronic inflammation Tuberculosis } Syphilis } Ruptured epidermoid cyst } Living agents Non-living agent Sarcoidosis } Unknown cause Rheumatoid arthritis } TUBERCULOSIS Caused by bacterium - tubercle bacillus. Usually hominis strain. May also be caused by bovis and various atypical mycobacteria. Stages 1 First infection - transient acute inflammatory reaction. 2 Early tubercle granuloma in lung - giant cells, epithelioid cells, lymphocytes, peripheral fibroblasts. 3. Ghon focus - formation of several granulomas. 4. Ghon complex - subpleural focus in lung and development of granulomas in regional lymph nodes. 5. Development of delayed hypersensitivity leads to one of three courses: i) healing by fibrosis ii) progression of chronic form, or iii) disseminated tuberculous granulomas throughout body (miliary spread) 6 Chronic tuberculosis can lead to either: i) healing leaving scar, ii) progression Progression may lead to:- bronchial erosion cavitation bronchopneumonia miliary spread

4 SYPHILIS Caused by spirochaete Treponema pallidum Primary syphilis 1. Initial infection and multiplication at site of entry 2. Spirochaetes enter regional lymph nodes 3. Spirochaetes enter many tissues, multiply, disseminate and sensitise tissues. 4. Primary sore or chancre forms at site of entry within 2-4 weeks of initial infection. Secondary syphilis 1. Low grade pyrexia 2. Lymphadenopathy 3. Skin rashes 4. Snail track ulcers Tertiary syphilis 1. Gummata - localised lesions most common in: hard palate liver testis 2. Diffuse lesions occur in:- a) cardiovascular system b) nervous system c) skeletal system RUPTURED EPIDERMOID CYST Cyst filled with keratin squames Inflammatory reaction in response to keratin if it ruptures, features:- giant cells macrophages plasma cells lymphocytes SARCOIDOSIS Chronic granulomatous systemic disease process of unknown aetiology. Lesions are similar to those of tuberculosis.

5 Histological Immunological Sarcoidosis no bacilli present no caseation giant cells may contain Schaumann bodies Mantoux negative Kveim test positive Tuberculosis bacilli present caseation giant cells do not contain Schaumann bodies Mantoux positive Kveim test negative RHEUMATOID ARTHRITIS Rheumatoid arthritis is a chronic progressive inflammatory arthritis of unknown origin involving multiple joints and characterised by a tendency to spontaneous remissions and subsequent relapses. The Rheumatoid lesion consists of: 1 Lymphocyte and plasma cell infiltration 2 Vasculitis 3 Rheumatoid nodules A rheumatoid nodule is composed of necrotic tissue and fibrin surrounded by a band of epithelioid cells and histiocytes and an outer zone of granulation tissue. It can be anything up to several cms in diameter. Pannus, which is really an overgrowth of granulation tissue, forms within the joints in rheumatoid arthritis and the underlying cartilage is destroyed, probably due to the destructive effects of lysosomal enzymes from polymorphs. Healing HEALING The replacement of lost and dead tissue by living tissue. PROCESSES IN HEALING (1) Resolution (2) Regeneration (3) Repair (1) Resolution

6 The scavenging of dead tissue and foreign material by macrophages. This is a preliminary to regeneration and repair. (2) Regeneration The replacement of lost and dead tissue by tissue similar in type. Regeneration only occurs when surviving cells of a tissue are capable of cell division. Examples of tissues capable of regeneration i) epithelial surfaces eg epidermis of skin ii) blood capillaries iii) some supporting tissue eg bone 3) Repair The replacement of lost and dead tissue by tissue of a different type, usually fibrous tissue. Healing by repair is inevitable in some tissues when cells are lost, eg muscle and nerve cells, which cannot regenerate. Healing by repair After damage to a tissue there is an acute inflammatory reaction in surrounding liver tissues, with formation of a blood clot if vessels have been damaged. Healing by repair occurs as follows. i) Macrophages in the inflammatory exudate scavenge fibrin, dead cells and other material. ii) Newly-formed capillaries grow into the area, accompanied by fibroblasts. iii) Fibroblasts do two things: they contract, which can reduce the extent of the damaged area, and they lay down collagen fibres. iv) Finally most capillaries and cells disappear leaving a mass of collagen ie fibrous tissue, or scar. Granulation tissue is the mixture of newly-formed capillaries, fibroblasts, macrophages and other inflammatory cells, which grows into an area of acute inflammatory exudate. Organisation is the resolution and repair of dead tissue or a thrombus. SPECIFIC EXAMPLES OF HEALING Tissue Method of Healing 1) Heart muscle Repair 2) Bone Regeneration, sometimes repair 3) Skin Regeneration of epidermis and repair of dermis

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