RNAscope: A Novel in Situ RNA Analysis Platform for Formalin-Fixed, Paraffin-Embedded Tissues

The Sensory Neurons of Touch

http://www.endoexperience.com/documents/Cellularmolecularandtissuelevelreactionstoorthoforce_2006.pdf

Cellular, molecular, and tissue-level reactions to orthodontic force

Teeth move through alveolar bone, whether through the normal process of tooth eruption or by strains generated by orthodontic appliances. Both eruption and orthodontics accomplish this feat through similar fundamental biological processes, osteoclastogenesis and osteogenesis, but there are differences that make their mechanisms unique. A better appreciation of the molecular and cellular events that regulate osteoclastogenesis and osteogenesis in eruption and orthodontics is not only central to our understanding of how these processes occur, but also is needed for ultimate development of the means to control them. Possible future studies in these areas are also discussed, with particular emphasis on translation of fundamental knowledge to improve dental treatments.

Mechanisms of Tooth Eruption and Orthodontic Tooth Movement

Previously, we discovered that periodontal ligament (PDL) cells not only support osteoclastogenesis through cell-to-cell contact, but also inhibit the formation of tartrate-resistant acid phosphatase-positive (TRAP+) multinucleated cells by a producing soluble factor(s). Furthermore, PDL cells express both receptor activator of nuclear factor kappaB ligand (RANKL) and osteoprotegerin (OPG) messenger RNA (mRNA). Clinically, "ankylosed teeth," which lack periodontal ligament, cannot be moved with orthodontic tooth treatment. From this, we hypothesized that PDL cells under mechanical stress should play a pivotal role in osteoclast formation during orthodontic tooth movement. This study examined how mechanical stress affects the osteoclastogenesis-supporting activity of PDL cells. PDL cells were compressed continuously and then cocultured with peripheral blood mononuclear cells (PBMCs) for 4 weeks. PDL cells under mechanical stress up-regulated osteoclastogenesis from PBMCs. Furthermore, the expression of RANKL mRNA and protein in PDL cells increased with compressive force in parallel with the change in the number of osteoclasts. In addition, cyclo-oxygenase 2 (COX-2) mRNA expression was induced by compressive force, and indomethacin inhibited the RANKL up-regulation resulting from compressive force. PDL cells under compressive force exhibited significantly increased prostaglandin E2 (PGE2) production in comparison with control PDL cells. Exogenous PGE2 treatment increased RANKL mRNA expression in PDL cells. Interestingly, OPG expression remained constant throughout compressive force or PGE2 treatment. In conclusion, compressive force up-regulated RANKL expression in PDL cells. Furthermore, RANKL up-regulation in mechanically stressed PDL cells was dependent on PGE2.

Periodontal Ligament Cells Under Mechanical Stress Induce Osteoclastogenesis by Receptor Activator of Nuclear Factor κB Ligand Up-Regulation via Prostaglandin E2 Synthesis†

Effects of bimaxillary surgery and mandibular setback surgery on pharyngeal airway measurements in patients with Class III skeletal deformities.

Progressive condylar resorption is an irreversible complication and a factor in the development of late skeletal relapse after orthognathic surgery. We have evaluated cephalometric characteristics, signs and symptoms in the temporomandibular joint (TMJ), and surgical factors in six patients (one man and five women) who developed it after orthognathic surgery. The findings in preoperative cephalograms indicated that the patients had clockwise rotation of the mandible and retrognathism because of a small SNB angle, a wide mandibular plane angle, and a "minus" value for inclination of the ramus. There were erosions or deformities of the condyles, or both, on three-dimensional computed tomography (CT) taken before treatment. The mean (SD) anterior movement of the mandible at operation was 12.1 (3.9)mm and the mean relapse was -6.4 (2.5)mm. The mean change in posterior facial height was 4.5 (2.1)mm at operation and the mean relapse was -5.3 (1.8)mm. Two patients had click, or pain, or both, preoperatively. The click disappeared in one patient postoperatively, but one of the patients who had been symptom-free developed crepitus postoperatively. In the classified resorption pattern, posterior-superior bone loss was seen in three cases, anterior-superior bone loss in two, and superior bone loss in one. Progressive condylar resorption after orthognathic surgery is multifactorial, and some of the risk factors are inter-related. Patients with clockwise rotation of the mandible and retrognathism in preoperative cephalograms; erosion, or deformity of the condyle, or both, on preoperative CT; and wide mandibular advancement and counterclockwise rotation of the mandibular proximal segment at operation, seemed to be at risk. The mandible should therefore be advanced only when the condyles are stable on radiographs, and careful attention should be paid to postoperative mechanical loading on the TMJ in high-risk patients.

Isao Saito

Papers

Effects of bimaxillary surgery and mandibular setback surgery on pharyngeal airway measurements in patients with Class III skeletal deformities.

Progressive condylar resorption after mandibular advancement.

Long-term observation of autotransplanted teeth with complete root formation in orthodontic patients.

Soft-tissue cephalometric norms in Yemeni men

Responses of calcitonin gene-related peptide-immunopositive nerve fibres in the periodontal ligament of rat molars to experimental tooth movement.