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Identification of cellular and matrix changes in paradental tissues following the application of orthodontic forces led to histochemical studies aimed at elucidating enzymes that might participate in this remodeling process. In 1983, Lilja, Lindskog, and Hammarström reported on the detection of various enzymes in mechanically strained paradental tissues of rodents, including acid and alkaline phosphatases, β‐galactosidase, aryl transferase, and prostaglandin synthetase. Meikle et al. (1989) stretched rabbit coronal sutures in vitro, and recorded increases in the tissue concentrations of metalloproteinases, such as collagenase and elastase, and a concomitant decrease in the levels of tissue inhibitors of this class of enzymes. Davidovitch et al. (1976, 1978, 1980a, b, c, 1992, 1996) used immunohistochemistry to identify a variety of first and second messengers in cats’ mechanically stressed paradental tissues in vivo. These molecules included cyclic nucleotides, prostaglandins, neurotransmitters, cytokines, and growth factors. Computer‐aided measurements of cellular staining intensities revealed that paradental cells are very sensitive to the application of orthodontic forces, that this cellular response begins as soon as the tissues develop strain, and that these reactions encompass cells of the dental pulp, PDL, and alveolar bone marrow cavities. Figure 1.16 shows a cat maxillary canine section, stained immunohistochemically for prostaglandin E₂ (PGE₂), a 20‐carbon essential fatty acid, produced by many cell types and acting as a paracrine and autocrine. This canine was not treated orthodontically (control). The PDL and alveolar bone surface cells are stained lightly for PGE₂. In contrast, 24 hours after the application of force to the other maxillary canine, the stretched cells (Figure 1.17) stain intensely for PGE₂. The staining intensity is indicative of the cellular concentration of the antigen in question. In the case of PGE₂, it is evident that orthodontic force stimulates the target cells to produce higher levels than usual of PGE₂. Likewise, these forces increase significantly the cellular concentrations of cyclic AMP, an intracellular second messenger (Figures ), and of the cytokine interleukin‐1β (IL‐1β), an inflammatory mediator, and a potent stimulator of bone resorption (Figures 1.21 and 1.22).

Figure 1.16 A 6 μm sagittal section of a cat maxilla, unfixed and nondemineralized, stained immunohistochemically for PGE₂. This section shows the PDL‐alveolar bone interface near one canine that received no orthodontic force (control). PDL and alveolar bone surface cells are stained lightly for PGE₂.