NECROSISNecrosis is defi ned as a localised area of death of tissue followed later by degradation of tissue by hydrolytic enzymes liberated from dead cells; it is invariably accompanied by inflamatory reaction.

Necrosis can be caused by various agents such as hypoxia, chemical and physical agents, microbial agents, immunological injury, etc.

Based on etiology and morphologic appearance, there are 5 types of necrosis:

coagulative, liquefaction (colliquative), caseous, fat, fibrinoid necrosis.

1. COAGULATIVE NECROSIS Th is is the most common type of necrosis caused by irreversible focal injury, mostly from sudden cessation of blood flow (ischaemic necrosis), and less often from bacterial and chemical agents. Th e organs commonly aff

the hallmark of coagulative necrosis is the conversion of normal cells into their ‘tomb stones’ i.e. outlines of the cells are retained and the cell type can still be recognised but their cytop lasmic and nuclear details are lost.

LIQUEFACTION (COLLIQUATIVE) NECROSIS Liquefaction or colliquative necrosis also occurs commonly due to ischaemic injury and bacterial or fungal infections but hydrolytic enzymes in tissue degradation have a dominant role in causing semi-fluid material. The common examples are infarct brain and abscess cavity.

The affected area is soft with liquefied centre containing necrotic debris. Later, a cyst wall is formed. the cystic space contains necrotic cell debris and macrophages filled with phagocytosed material.

CASEOUS NECROSIS Caseous (caseous= cheese-like) necrosis is found in the centre of foci of tuberculous infections. It combines features of both coagulative and liquefactive necrosis.

Foci of caseous necrosis resemble dry cheese and are soft, granular and yellowish. Th is appearance is partly attributed to the histotoxic eff ects of lipopolysaccharides present in the capsule of the tubercle bacilli, Mycobacterium tuberculosis.

FAT NECROSIS Fat necrosis is a special form of cell death occurring at mainly fat-rich anatomic locations in the body. The examples are: traumatic fat necrosis of the breast, especially in heavy and pendulous breasts, and mesenteric fat necrosis due to acute pancreatitis.

In fat necrosis, there is hydrolysis and rupture of adipocytes, causing release of neutral fat which changes into glycerol and free fatty acids. The leaked out free fatty acids complex with calcium to form calcium soaps (saponification).

FIBRINOID NECROSIS Fibrinoid necrosis is characterized by deposition of fi brin-like material which has the staining properties of fi brin such as phosphotungistic acid haematoxylin (PTAH) stain. It is encountered in various examples of immuno logic tissue injury (e.g. in immune complex vasculitis, autoimmune diseases, Arthus reaction etc), arterio les in hypertension, peptic ulcer etc.

Pulp necrosis - Pulp Necrosis is a clinical diagnostic category indicating death of the dental pulp, necessitating root canal treatment.

A necrotic pulp should be suspected when the tooth does not respond to pulp sensibility tests. However, this will not always be the case since teeth with pulp canal calcification, previous root fillings or pulpotomies will also not respond to pulp sensibility tests.

It is important to realize that a necrotic pulp per se does not cause apical periodontitis unless it is infected.21-23 Pain usually does not present unless the periodontal ligament is affected.

Once a necrotic pulp is invaded by bacteria, then the bacteria will spread throughout the entire root canal system. The necrotic pulp acts as a source of nutrients for the bacteria which ingest the necrotic tissue and render the tooth pulpless. This may occur within 1–2 months of the initial invasion by the bacteria.