John M. Crawford

Minor salivary glands as a major source of secretory immunoglobin A in the human oral cavity

Secretory immunoglobulin A is the predominant immunoglobulin in labial minor salivary gland secretions. Its mean concentration is four times higher in these secretions than in parotid gland secretion. The minor salivary glands can produce 30 to 35 percent of the immunoglobulin A that enters the oral cavity. This, together with the potential accessibility of these glands to antigenic stimulation, suggest that they may be an important source of the immune factors that are involved in the regulation of the microorganisms in the oral environment.

Cell Adhesion Molecules in Inflammation and Immunity: Relevance to Periodontal Diseases:

Inflammatory and immune responses involve close contact between different populations of cells. These adhesive interactions mediate migration of cells to sites of inflammation and the effector functions of cells within the lesions. Recently, there has been significant progress in understanding the molecular basis of these intercellular contacts. Blocking interactions between cell adhesion molecules and their ligands has successfully suppressed inflammatory reactions in a variety of animal models in vivo. The role of the host response in periodontal disease is receiving renewed attention, but little is known of the function of cell adhesion molecules in these diseases. In this review we summarize the structure, distribution, and function of cell adhesion molecules involved in inflammatory/immune responses. The current knowledge of the distribution of cell adhesion molecules is described and the potential for modulation of cell adhesion molecule function is discussed.

Characterization of Immunoglobulin-Containing Cells in the Submandibular Gland of the Rat after Local Immunization

The large lymphocytes which enter the blood via the thoracic duct lymph have been shown to migrate selectively into the lamina propria of the small intestine (1). These cells are presumably derived from the Peyer’s patches and components of the gut-associated lymphoid tissue (GALT) (2). Recent reports have suggested that cells derived from the GALT may also “home” to other secretory tissues including the mammary (3) and salivary glands (4), It has been demonstrated that lymphocytes, in response to antigens, are recruited from the blood into the local lymph node and during this phase both antibody and nonantibody-secreting precursor cells are recruited into the node (5). Similarly, after migration of IgA precursor cells to the local secretory tissue, differentiation into IgA-synthesizing cells may occur upon contact with antigen. However, quantitative information on the induction of antibody synthesis at the cellular level in exocrine tissues (e.g., salivary glands) is sparse and is usually obtained from examination of fixed tissue sections (6). We have begun a series of studies into aspects of the secretory immune responses in the oral cavity by developing a method for isolation of mononuclear cells from the submandibular gland (SMG) of the rat.

A longitudinal study of unsaturated iron-binding capacity and lactoferrin in unstimulated parotid saliva

Availability of iron is one important nutritional parameter for microbial growth in saliva. This longitudinal study measured the diurnal and day-to-day variations in the total iron (TI), total ironbinding capacity (TIBC), unsaturated iron-binding capacity (UIBC), and lactoferrin (LF) in unstimulated human parotid saliva. Saliva was collected from 15 young male subjects in the morning and afternoon hours each day for five consecutive days. The TI and TIBC were determined by flameless atomic absorption spectroscopy, and UIBC was determined by subtraction of TI from TIBC. The LF was determined by “sandwich” enzyme-linked immunosorbent assay (ELISA). One peripheral blood sample of each subject was also analyzed for TI, TIBC, and ferritin. The results showed no significant diurnal or day-to-day variation of TI, TIBC, UIBC, or LF in saliva for most subjects. However, significant between-subject variations were observed for most parameters. Variations ranged from subjects with constantly positive UIBC values to subjects with constantly negative UIBC values. The relationship between the LF values and the TI and TIBC values suggests that other iron-binding protein(s) are present in saliva. Also, saliva had significantly lower TIBC values than serum. This finding indicated that iron may be easily available in saliva. However, further studies are required to determine the relationship between UIBC value of saliva and oral and dental diseases, and also to detect the presence of other iron-binding proteins in saliva.

Periodontitis and Cardiovascular Disease

John M. Crawford, BDS, PhD roundbreaking studies in the 1980s demonstrated the causative role of eliobacter pylori in gastric and duodenal ulceration. These findings timulated an explosion of research into the possible microbial etiologies f a variety of other prevalent diseases and conditions—as described in ther articles in this volume. This article briefly reviews studies that have nvestigated the relationship between periodontal infections and atheroclerotic disease of coronary arteries (atherosclerotic cardiovascular isease—ACD). Current evidence based, in part, on several recent eta-analyses of cross-sectional studies (of varying experimental design) n patients with ACD and periodontitis (and a number of surrogate arkers for these diseases) have confirmed the association between the 2 iseases. This relationship appears to be independent of other known isk factors. However, the strength of the association appears to be elatively modest, with odds ratio estimates ranging from 1.24 to 1.34. he studies included in these meta-analyses are heterogeneous, and ariations in risk have been reported among different ethnic groups and ubjects in different age groups. Additional sources of heterogeneity are he different measures used to diagnose periodontitis and ACD. Many nvestigators caution that we do not have evidence that the 2 diseases are ausally related and emphasize that we need well-designed longitudinal tudies to demonstrate causality. With both ACD and periodontitis, it is ifficult to diagnose the onset of disease, making the relationship between he 2 diseases even more difficult to unravel. So, at this time, we are not n a position to claim a cause-and-effect relationship between periodonitis and ACD. A recent consensus statement by the editors of the merican Journal of Cardiology and the Journal of Periodontology larifies this point by stating: “A direct causal relation between periodonitis and atherosclerotic CVD is not established.” If we accept that there is a real but modest association between eriodontitis and ACD, what mechanisms could be responsible for the ssociation? Most discussions refer to the possibility of direct and indirect