The anterior cruciate ligament (ACL) inserts into bone through a characteristic fibrocartilagenous interface, which is essential for load transfer between soft and hard tissues. This multi-tissue interface is lost post ACL reconstruction, and the lack of an anatomic fibrocartilage interface between graft and bone remains the leading cause of graft failure. Currently, the mechanism of interface formation is not known. As a fibrocartilage-like tissue is found within the bone tunnel post ACL reconstruction, we hypothesize that fibroblast-osteoblast interactions at the graft-to-bone junction play a role in fibrocartilage formation. To test this hypothesis, a coculture model permitting osteoblast-fibroblast communications was used to determine the effects of heterotypic interactions on cell phenotype and the development of fibrocartilage-relevant markers in vitro. It was found that co-culture decreased cell proliferation and osteoblastmediated mineralization, while inducing fibroblast-mediated mineralization. Moreover, the expression of interface-relevant markers such as collagen type II and aggrecan were detected. Our findings suggest that osteoblast-fibroblast interactions may lead to cell trans-differentiation and eventual fibrocartilage formation. These results provide new insight into the mechanism of fibrocartilage formation, which are critical for interface tissue engineering and achieving biological fixation of soft tissue grafts to bone. ß
The initial secondary cellular changes detected in the rodless tadpole retina mimic those observed in other models of retinal degeneration. The rapid and synchronous rod loss in XOPNTR animals suggested this model may prove useful in the study of retinal degeneration. Moreover, the regenerative capacity of the Xenopus retina makes these animals a valuable tool for identifying the cellular and molecular mechanisms at work in lower vertebrates with the remarkable capacity of retinal regeneration.
Purpose Analysis of macular pigment (MP) amount and distribution in patients with macular telangiectasia type 2 (MacTel) receiving oral zeaxanthin supplementation in a randomized, open-label interventional trial. Methods Eight MacTel patients were randomized to 10 mg or 20 mg of zeaxanthin per day. At each visit, the subjects were examined including best corrected visual acuity (BCVA), contrast sensitivity (CS), fundus biomicroscopy, color fundus photography (CFP), autofluorescence imaging (AFI), optical coherence tomography (OCT), and serum carotenoid levels. Patients were assessed at baseline and after 6, 12, 18, and 24 months of zeaxanthin supplementation. MP concentration was analyzed and calculated from AFI obtained at 488 nm excitation wavelength. Serum carotenoid levels were obtained using high-performance liquid chromatography (HPLC). Results The majority of subjects had definite increases in intensity of the macular pigment’s hypofluorescent ring, but none of them deposited macular pigment centrally at the fovea. Although some patients noted subjective improvements in vision, no objective improvements could be documented, and there were no changes in foveal OCT features. Yellowish, hypofluorescent crystals appeared in one subject’s macular region with no change in visual acuity. These inner retinal crystals disappeared several months after discontinuing her 20 mg zeaxanthin supplement. Conclusion Based on our study, zeaxanthin supplementation does not result in any visual benefit in patients with MacTel, and does not re-establish a normal peaked distribution of macular pigment in the fovea. One subject developed a novel, reversible crystalline maculopathy in response to zeaxanthin supplementation that was reminiscent of canthaxanthin crystalline maculopathy.
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