Question Set 1. What are the important destructive mechanisms in periodontal diseases? 2. What are the important protective mechanisms in periodontal diseases? 3. What are the important genetic factors and what is the state-of-the art relative to assessing these genetic factors in periodontal diseases? 4. What do we know about the mechanism of action of possible risk factors, such as smoking and diabetes on the host? 5. What is the evidence that host modulating agents will be effective in prevention or treatment ofperiodontal diseases?

Periodontal diseases: pathogenesis.

The identification of cytokines, a class of intermediate molecular weight, intercellular regulatory proteins, and an understanding of their function has been facilitated tremendously by the use of recombinant DNA technology. Following closely upon these developments has come the ability to detect and quantify cytokines in clinical and biological samples, in large part made possible by the use of specific and sensitive immunoassays using anti-cytokine antibodies. Cytokine detection with antibody-based techniques is particularly useful because so many of these factors have overlapping, parallel, or counter-regulatory bioactivities and it is extremely difficult to distinguish and measure them in complex mixtures on the basis of biological activity alone, Therefore, both neutralizing antibodies in bioassay systems and cytokine immunoassays of complex samples are required (Mosmann & Fong 1989). In the first part of this review, we outline the general strategy we have followed for preparing a large panel of anti-mouse and human cytokine monoclonal antibodies (mAb) and setting up cytokine immunoassays. While there is a general consensus that many of the frequently produced cytokines such as IL-1, TNF, IFN-y, IL-6, and IL-8 may be general inflammatory mediators, see for example (Dunn 1991), definitive links between the detection of specific cytokine patterns and the pathogenesis of particular diseases are in the early stages of being understood. The eventual elucidation of such cause-and-

Strategies of anti-cytokine monoclonal antibody development: immunoassay of IL-10 and IL-5 in clinical samples.

Alterations have been found to occur in every component of immune response during anaesthesia and surgery. These alterations represent the body's general physiological responses and are mainly dependent on the extent of surgery, as well as other factors such as the patient's age and health status, medication and blood transfusion. Anaesthetic and operative complications have profound effects on these responses. Basically, the immune response to anaesthesia and surgery is a beneficial reaction, needed in local host defences and wound healing and in preventing the body from making autoantibodies against its own tissues. The responses may, however, contribute to the development of postoperative infections and spread of malignant disease. During uncomplicated conventional surgery, the immune response usually passes clinically unnoticed without any harmful effects. Absent responses and excessively high responses, on the other hand, harm the patient. Our understanding of immunological phenomena and our possibilities of controlling mediator activation are now lagging behind the technical advances made in operative treatment. If we want to decrease operative morbidity and mortality to below their present levels, more attention should be directed to immune responses to major surgery, injuries and operative complications with massive mediator release which place the surgical patient at risk. Experimental evidence suggests that results of treatment in injured and operated patients can in the future be improved by controlling immune responses and their mediator systems. Our current level of knowledge of immune responses is already helping us to avoid many immune-mediated complications. However, routine interference with these responses is not indicated.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1399-6576.1992.tb03452.x

Effects of anaesthesia and surgery on the immune response.

Assessment of protein energy malnutrition in older persons, Part II: Laboratory evaluation.

The epithelium has long been regarded as a passive barrier intended to protect the underlying tissues. Many regulatory signals, including cytokines, that control epithelial cell proliferation and differentiation and cell function during inflammation were thought to be nonepithelial-derived. Now there is a growing appreciation that epithelial cells provide some of the impetus for their own growth and differentiation, and may also regulate the function of other cells through the elaboration of certain cytokines. Moreover, because epithelial cells serve as the interface between the organism and environment, they are in a position to signal changes in the environment. It is now clear that epithelial cells respond to injury or infection with cytokine secretion. Various approaches to detecting cytokines in normal and diseased tissue have been undertaken during the past few years to establish cytokine synthesis by different epithelial. This review will examine these recent investigations in various general contexts of epithelial cell function.

Cytokine production by epithelial cells.

Cytokines are peptides used by immune and inflammatory cells to communicate with each other and to control the milieu interieur in which they operate. Recent evidence suggests that they are of immense importance in controlling the local and systemic events of the immune response, inflammation, hemopoiesis, healing, and the systemic response to injury. Many of them can now be measured by immunoassay, and the role of such measurements in the diagnosis and management of disease is actively under investigation. Similarly, the availability of recombinant DNA techniques to produce cytokines in almost unlimited quantities is leading to new and exciting therapeutic applications.

S W Evans

Papers

Cytokines in disease.