Page 186 - Textbook of Pathology, 6th Edition

170 5. Incisional hernia. A weak scar, especially after a i) Fibronectin (nectere = to bind) is the best characterised
laparotomy, may be the site of bursting open of a wound glycoprotein in ECM and has binding properties to other cells
(wound dehiscence) or an incisional hernia. and ECM. It is of two types—plasma and tissue fibronectin.
6. Hypertrophied scars and keloid formation. At times the scar Plasma fibronectin is synthesised by the liver cells and is
formed is excessive, ugly and painful. Excessive formation trapped in basement membrane such as in filtration through
of collagen in healing may result in keloid (claw-like) the renal glomerulus.
formation, seen more commonly in Blacks. Hypertrophied Tissue fibronectin is formed by fibroblasts, endothelial
scars differ from keloid in that they are confined to the cells and other mesenchymal cells. It is responsible for the
borders of the initial wound while keloids have tumour-like primitive matrix such as in the foetus, and in wound healing.
SECTION I
projection of connective tissue.
ii) Tenascin or cytotactin is the glycoprotein associated with
7. Excessive contraction. An exaggeration of wound fibroblasts and appears in wound about 48 hours after injury.
contraction may result in formation of contractures or It disappears from mature scar tissue.
cicatrisation e.g. Dupuytren’s (palmar) contracture, plantar iii) Thrombospondin is mainly synthesised by granules of
contracture and Peyronie’s disease (contraction of the platelets. It functions as adhesive protein for keratinocytes
cavernous tissues of penis).
and platelets but is inhibitory to attachment of fibroblasts
8. Neoplasia. Rarely, scar may be the site for development and endothelial cells.
of carcinoma later e.g. squamous cell carcinoma in Marjolin’s
ulcer i.e. a scar following burns on the skin. 3. BASEMENT MEMBRANE. Basement membranes are
periodic acid-Schiff (PAS)-positive amorphous structures
Extracellular Matrix— Wound Strength that lie underneath epithelia of different organs and
endothelial cells. They consist of collagen type IV and
The wound is strengthened by proliferation of fibroblasts laminin.
and myofibroblasts which get structural support from the
extracellular matrix (ECM). In addition to providing 4. ELASTIC FIBRES. While the tensile strength in tissue
structural support, ECM can direct cell migration, comes from collagen, the ability to recoil is provided by elastic
attachment, differentiation and organisation. fibres. Elastic fibres consist of 2 components—elastin
ECM has five main components: collagen, adhesive glycoprotein and elastic microfibril. Elastases degrade the
glycoproteins, basement membrane, elastic fibres, and elastic tissue e.g. in inflammation, emphysema etc.
proteoglycans.
5. PROTEOGLYCANS. These are a group of molecules
1. COLLAGEN. The collagens are a family of proteins having 2 components—an essential carbohydrate polymer
General Pathology and Basic Techniques
which provide structural support to the multicellular (called polysaccharide or glycosaminoglycan), and a protein
organism. It is the main component of tissues such as fibrous bound to it, and hence the name proteo-glycan. Various
tissue, bone, cartilage, valves of heart, cornea, basement proteoglycans are distributed in different tissues as under:
membrane etc. i) Chondroitin sulphate—abundant in cartilage, dermis
Collagen is synthesised and secreted by a complex ii) Heparan sulphate—in basement membranes
biochemical mechanism on ribosomes. The collagen synthesis iii) Dermatan sulphate—in dermis
is stimulated by various growth factors and is degraded by iv) Keratan sulphate—in cartilage
collagenase. Regulation of collagen synthesis and v) Hyaluronic acid—in cartilage, dermis.
degradation take place by various local and systemic factors In wound healing, the deposition of proteoglycans
so that the collagen content of normal organs remains precedes collagen laying.
constant. On the other hand, defective regulation of collagen The strength of wound also depends upon factors like
synthesis leads to hypertrophied scar, fibrosis, and organ the site of injury, depth of incision and area of wound. After
dysfunction. removal of stitches on around 7th day, the wound strength
Depending upon the biochemical composition, 18 types is approximately 10% which reaches 80% in about 3 months.
of collagen have been identified called collagen type I to XVIII,
many of which are unique for specific tissues. Type I collagen TURNOVER OF ECM. ECM is not a static structure but
is normally present in the skin, bone and tendons and the matrix proteins comprising it undergo marked
accounts for 90% of collagen in the body: remodeling during foetal life which slows down in adult
Type I, III and V are true fibrillar collagen which form the tissues. These matrix proteins are degraded by a family of
main portion of the connective tissue during healing of metalloproteinases which act under regulatory control of
wounds in scars. inhibitors of metalloproteinases.
Other types of collagen are non-fibrillar and amorphous
material seen as component of the basement membranes. Factors Influencing Healing
Morphologically, the smallest units of collagen are Two types of factors influence the wound healing: those
collagen fibrils, which align together in parallel bundles to acting locally, and those acting in general.
form collagen fibres, and then collagen bundles.
2. ADHESIVE GLYCOPROTEINS. Various adhesive A. LOCAL FACTORS:
glycoproteins acting as glue for the ECM and the cells consist 1. Infection is the most important factor acting locally which
of fibronectin, tenascin (cytotactin) and thrombospondin. delays the process of healing.