Chapter 2 Patterns of growth in health and disease
The growth of cells and tissues is an essential normal process. Cells and tissues possess a defined lifespan and the continued survival of the whole individual is dependent upon the successful removal and replacement of effete (i.e. worn out) cells with new counterparts. Tissues also require the capacity to change their size in response to a wide range of physiological stimuli:
Changes to the normal mechanisms governing tissue kinetics can result in abnormal tissue growth and the development of neoplasia (Chs 20–25) as well as many aspects of non-neoplastic disease (e.g. an abnormally enlarged heart).
Normal cellular kinetics
Almost all tissues undergo a normal physiological process of cellular ‘management’ that involves the removal of effete or damaged cells and their replacement by new mature cells. The rate of cellular turnover is extremely variable between tissues. Tissues possessing the highest rates of turnover include the bone marrow and the epithelial cells lining the gastrointestinal tract. These tissues show the highest rates of cell division and are, therefore, the most susceptible to ‘collateral’ damage by chemotherapeutic treatments that inhibit cell division. Microscopic examination of biopsy samples from these tissues reveals easily identifiable evidence of cell division (i.e. mitotic figures) in normal situations. Many other tissues show a much lower rate of cell turnover but retain the ability to increase in size by cell division when required. The best example of this is the liver, which can return to a normal size even after partial surgical hepatectomy. Some mature tissues possess little or no capacity for cell division. The prime example is central nervous tissue, which also is essentially made up of cells with no extracellular connective tissue matrix. These combined features lead to the limited capacity for recovery from major insults such as extensive cerebral infarction, which is established by detecting a cystic space within the brain. Another example is the heart, with myocardial cell death (e.g. in infarction) leading to healing by fibrous scar tissue formation rather than complete repair via cardiac myocyte cell division. This means that extensive myocardial infarction commonly interferes significantly with the contractile ability of the left ventricle and, therefore, predisposes to heart failure.