Page 698 - Veterinary Immunology, 10th Edition

a mucosal “firewall” must be established to discourage invasion.
VetBooks.ir infections. Small amounts of IgG are secreted into the crevicular
Saliva is rich in IgA and hence protects the mouth against

groove between the gums and the base of the teeth. As a result, it

has proved possible to make a vaccine against caries-causing
bacteria (Box 22.1). Immunization of dogs with these organisms
reduces microbial colonization of this area and prevents plaque
formation and periodontitis. The flushing activity of saliva may be

complemented by the generation of peroxidases from streptococci.
The tonsils also produce much IgA, but because of the thin
epithelium over the tonsillar clefts, they are very vulnerable to
microbial invasion (Fig. 22.5).

Box 22.1

Periodontal Disease

Gingivitis and progressive chronic periodontitis are common
diseases in animals. The tissue damage that occurs in periodontal

disease is mediated by cells of the immune and inflammatory
systems. The disease is triggered by many oral bacteria, the most
important of which is Porphyromonas gingivalis. But the tooth

microbiota are diverse and the composition of the population
varies over time. These bacteria form biofilms on the surface of
dental plaque. The PAMPs from these bacteria act through TLRs
and other PRRs to attract neutrophils. The neutrophils, however,
cannot phagocytose biofilms, so they undergo abortive

phagocytosis and release their contents into the tissues. These
released enzymes, especially collagenases, initiate progressive
tissue destruction. In addition, local mast cells secrete TNF-α that

contributes to neutrophil immigration. The gingival fluid contains
complement components, especially C3a and C5a. The biofilm
ensures that inflammation persists and chronic inflammation leads
to chronic tissue destruction. Neutrophils are followed by
macrophages and lymphocytes by about four to seven days. By

day 21, 70% of the cellular infiltrate consist of lymphocytes, mainly
+
T cells. CD4 cells increase progressively through the course of the
disease and the lesion resembles a delayed hypersensitivity

reaction (Chapter 33). Th1 and Th17 cells predominate. The Th17

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