Clinical success of guided tissue regeneration for treating vertical bone and furcation defects in dogs.

This study evaluated the clinical success rate of guided tissue regeneration (GTR) for treating advanced periodontal disease in a large canine cohort. A total of 112 GTR procedures performed from 2003-2021 were retrospectively evaluated, including pre- and post-treatment (3-12 months) periodontal probing depths of 104 treated teeth, dental radiographs of 73 treated teeth, and both diagnostic modalities in 64 treated teeth. Probing depth, radiographically apparent bone height, bone graft material, barrier membrane material, and tooth extraction adjacent to the GTR site were investigated as factors affecting success. Vertical bone defects were evaluated separately from furcation defects. GTR was clinically successful, defined as objective improvement in probing depth, objective decrease in radiographic vertical bone defect, and subjective radiographic gain in bone height in 90.3% of vertical bone defects. Success was significantly associated with the magnitude of initial probing depth and the type of barrier membrane used. GTR was clinically successful, defined as objective improvement in furcation probing and subjective radiographic improvement of the bone in the furcation in 22.2% of furcation defects. When F3 lesions were excluded, GTR was successful in 64.3% of furcation defects. GTR is an appropriate treatment to maintain teeth in the oral cavity of dogs with proper client counseling and patient selection, but it is most likely to be successful in vertical defects.

Targeting VE-PTP activates TIE2 and stabilizes the ocular vasculature.

Retinal and choroidal neovascularization (NV) and vascular leakage contribute to visual impairment in several common ocular diseases. The angiopoietin/TIE2 (ANG/TIE2) pathway maintains vascular integrity, and negative regulators of this pathway are potential therapeutic targets for these diseases. Here, we demonstrated that vascular endothelial-protein tyrosine phosphatase (VE-PTP), which negatively regulates TIE2 activation, is upregulated in hypoxic vascular endothelial cells, particularly in retinal NV. Intraocular injection of an anti-VE-PTP antibody previously shown to activate TIE2 suppressed ocular NV. Furthermore, a small-molecule inhibitor of VE-PTP catalytic activity (AKB-9778) activated TIE2, enhanced ANG1-induced TIE2 activation, and stimulated phosphorylation of signaling molecules in the TIE2 pathway, including AKT, eNOS, and ERK. In mouse models of neovascular age-related macular degeneration, AKB-9778 induced phosphorylation of TIE2 and strongly suppressed NV. Ischemia-induced retinal NV, which is relevant to diabetic retinopathy, was accentuated by the induction of ANG2 but inhibited by AKB-9778, even in the presence of high levels of ANG2. AKB-9778 also blocked VEGF-induced leakage from dermal and retinal vessels and prevented exudative retinal detachments in double-transgenic mice with high expression of VEGF in photoreceptors. These data support targeting VE-PTP to stabilize retinal and choroidal blood vessels and suggest that this strategy has potential for patients with a wide variety of retinal and choroidal vascular diseases.