Teaching undergraduates the pathogenesis of periodontal disease is not an easy task. It is demanding for students and the teacher as well, who needs to integrate traditional knowledge about pathohistological features of the initial, early, and established lesions in the gingiva which may or may not develop into destructive periodontal disease with an understanding of the more dynamic, non-linear, and hierarchical network of mechanisms which might be modeled as interplay between microbes aggregated in a biofilm on the tooth surface and host reactions which may largely be responsible for periodontal destruction. In the current curriculum, for instance, I could only dedicate one hour didactic teaching on the topic which is, of course, a true challenge. Accordingly, learning goals [pdf] had been formulated which are not very explicit.
A new series of DVDs has been commenced by Quintessence Publishing on Cell-to-Cell Communications, and the second volume which follows Osseointegration is dedicated to Inflammatory Reactions. You may see the trailer when clicking here. As the preface by the two authors, H. Terheyden and B. Stadlinger, tells it was Alexander Ammann, “communication expert” and managing director of QuintPub, who had the original idea and who had “recognized the benefits of three-dimensional video animations for the visualization of complex biological relationships.”
Even at the microscopic scale of our body cells, the seemingly confusing communication networks and information flows can be made comprehensible by novel digital technologies. The human mind seems hardly able to comprehend biological networks as a whole. The protagonists of these networks are cells that communicate with each other via messenger molecules. Controlling our bodily functions – exemplified by inflammation and regeneration and periodontal disease – is not a hierarchical [sic] and monocausal process. Rather, a more successful descriptive model for these phenomena is that a host of interconnected control loops and equilibriums to be maintained.
Quintessence Publishing had “enlisted the assistance of InterActive Systems, Berlin, a group of video animation artists with a biological background.” Amazingly, authors mention that a “clear-cut distinction between the innate and adaptive immune system [had to be] made mainly for the purpose of didactic clarity, while in actual reality they overlap.”
An explicit aim of the series on Cell-to-Cell Communication was “to instill in students and other audiences a fascination with science.” Well, at least in that QuintPub failed gravely. Both bacteria and host cells are displayed all whitish-opaque making it difficult to differentiate them. While any dental student is soon familiar with a bewildering variety of different bacteria, be it gram-negative or -positive cocci, curved and straight rods, motile rods, filaments and fusiforms, and, in particular spirochetes, InterActive’s animation seem to have short rods in mind, sometimes roused by flagellated creatures which resemble those targeting heroes in Matrix Reloaded. Spirochetes, which may account for the majority of microorganisms in dental biofilm, seem to miss completely.
Do statements that “[t]he plaque prevents the inflow of the pellicle proteins that normally inhibit the crystallization of salivary mineral salts by keeping them in solution. Thus calculus forms,” make any sense? It is quite established that subgingival calculus does not have anything to do with salivary minerals. “In the deeper layers [of the biofilm] the bacterial flora shifts towards anaerobic, gram-negative and pathogenic strains.” Authors may realize that in the depth of the periodontal pocket at the surface of the biofilm, these bacteria may in fact elicit the respective response of the host. Bacteria in deeper layers are usually metabolically inactive, or may even be dead.
More serious errors occur in the 2nd chapter labelled the innate immune defense, apparently meaning complement, macrophages and neutrophils. In reality, neutrophils, which have left the blood stream, migrate through rather dense connective tissue and then junctional epithelium. In the movie, they just swim in an environment which largely resembles the small intestine. Fortunately, the voice-over mentions that these quickly swimming, submarine-like cells were neutrophils. Bacteria seem to have invaded the tissue already but are spectacularly attacked by the membrane attack complex (they just burst), something which won’t occur in the initial phases of gingival inflammation.
Very late in this video, even after the introduction of bone resorption which is very much characterized by dropping not further explained names of cytokines, the other chief characters appear, T-lymphocytes and plasma cells, as members of the adaptive immune system. One cannot, though, differentiate them, all are whitish and opaque. Here, communication should in fact be a topic, but the used language is not really comprehensible.
Naive T-Lymphocytes become antigen specific by contact with antigen presenting intra- and subepithelial dendritic cells. After repeated antigen exposure, antigen specific T-helper cells, the Th1 lymphocytes, synthesize amongst others [sic] large amounts of new soluble RANKL. This RANKL leads to osteoclast differentiation. This is mediated by interleukin-17 from Th-17 cells.
Another creature quickly swimming [the voice over speaks of “crawling”] in an unidentified environment leave fibers behind, and one instantly thinks of fibroblasts. This is actually the case when it comes to healing, after the doctor had removed the calculus with a scaler.
The inflammation is switched-off in a highly regulated cellular communication process, in which tissue inhibitors of metalloproteinases, lipoxins, resolvins and cytokine inhibitors [sic] are released.
I am afraid, the DVD won’t explain anything. Undergraduates won’t be fascinated by a 15-min crash course in immunology (and neither was I). The price of $98 is actually a bad joke.
22 February 2013 @ 1:50 pm.
Last modified February 22, 2013.