RANKL From Osteocytes Contributes to Periodontal Bone Loss

Periodontal bone loss results from bacterial infection and the associated host response. The ligand for the receptor activator of NF-κB (RANKL) induces the differentiation of osteoclasts, resulting in periodontal bone loss. The role of osteocytes in periodontal bone loss was investigated in this study. Transgenic mice expressing RANKL under the control of dentin matrix protein 1 (DMP1) were infected with Porphyromonas gingivalis- Fusobacterium nucleatum bacteria (Pg-Fn) to induce periodontitis, and type 1 diabetes was induced in groups of mice. Control (DMP1­Cre−.RANKLf/f) mice with periodontal infection showed increases in bone loss, osteoclast counts, eroded bone surfaces, and RANKL expression compared to experimental (DMP1-Cre+.RANKLf/f) mice. RANKL deletion from osteocytes resulted in less periodontal bone loss. Diabetes enhanced periodontal bone loss in the control mice. The diabetic control (DMP1­Cre−.RANKLf/f) mice had more bone loss than the non-diabetic control (DMP1­Cre−.RANKLf/f) mice. In the experimental (DMP1-Cre+.RANKLf/f) mice, diabetes had no influence. This study demonstrated, for the first time, the essential role of osteocytes in periodontal bone loss

RANKL Deletion in Periodontal Ligament and Bone Lining Cells Blocks Orthodontic Tooth Movement

The bone remodeling process in response to orthodontic forces requires the activity of osteoclasts to allow teeth to move in the direction of the force applied. Receptor activator of nuclear factor-κB ligand (RANKL) is essential for this process although its cellular source in response to orthodontic forces has not been determined. Orthodontic tooth movement is considered to be an aseptic inflammatory process that is stimulated by leukocytes inclduing T and B lymphocytes which are presumed to stimulate bone resorption. We determined whether periodontal ligament and bone lining cells were an essential source of RANKL by tamoxifen induced deletion of RANKL in which Cre recombinase was driven by a 3.2 kb reporter element of the Col1α1 gene in experimental mice (Col1α1.CreERTM+.RANKLf/f) and compared results with littermate controls (Col1α1.CreERTM-.RANKLf/f). By examination of Col1α1.CreERTM+.ROSA26 reporter mice we showed tissue specificity of tamoxifen induced Cre recombinase predominantly in the periodontal ligament and bone lining cells. Surprisingly we found that most of the orthodontic tooth movement and formation of osteoclasts was blocked in the experimental mice, which also had a reduced periodontal ligament space. Thus, we demonstrate for the first time that RANKL produced by periodontal ligament and bone lining cells provide the major driving force for tooth movement and osteoclastogenesis in response to orthodontic forces

High-Altitude Pulmonary Edema in Two Pediatric Patients with Pre-Existing Lung Disease

Background: The illnesses associated with changes in barometric pressure can be classified into three types: acute mountain sickness, high-altitude pulmonary edema (HAPE), and high-altitude cerebral edema. HAPE is a rare form of pulmonary edema that occurs in susceptible individuals after arriving at altitudes over 2500 m above sea level (m). Only a few studies have reported classical HAPE among children with underlying cardiopulmonary comorbidities. In this study, we report two pediatric cases of classical HAPE that occurred immediately upon arriving at Abha city (with an average elevation of 2270 m above sea level). Notably, both patients possessed underlying chronic lung diseases, raising crucial questions about susceptibility factors and the early onset manifestations of HAPE. Case: Two pediatric cases of HAPE are presented. The first patient, with a medical history of repaired right congenital diaphragmatic hernia and subsequent right lung hypoplasia, developed HAPE following their ascent to a high altitude. The second patient, diagnosed with diffuse lung disease of unknown etiology, experienced HAPE after a rapid high-altitude ascent. Both patients resided in low-altitude areas prior to ascent. The initial emergency room assessment revealed that both patients had severe hypoxia with respiratory distress that mandated the initiation of respiratory support and 100% oxygen therapy. They required intensive care unit admission, improved after 5 days of hospitalization, and were sent home in good condition. Conclusion: HAPE is a complex, potentially life-threatening high-altitude illness with diverse clinical presentations and variable risk factors. This case report sheds light on a potential predisposition factor—pre-existing lung disease—in children experiencing severe HAPE. While further validation is crucial, this valuable insight opens doors for improved preventative strategies and informed medical decisions for children with pre-existing lung conditions traveling to high altitudes