INTRODUCTION: Shrinkage is one of the complications observed after allograft meniscal transplantation. Subtle immune rejection and alterations in meniscal permeability leading to nutritional deficit have been suggested as causes of shrinkage. The purpose of this study was to ascertain how freezing, one of the most common procedures used to preserve allografts, alters the collagen’s architecture. METHODS: 26 fresh human external menisci were harvested in sterile conditions during TKR procedures. 13 of them were immediately frozen to −80° C while the rest were used as controls. All the menisci were cut, processed and preserved in a 2.0% glutaraldehyde and then analyzed with transmission electron microscopy. Four hundred collagen fibrils were recorded and measured in longitudinal and transversal sections in each meniscus. According to the collagen’s periodicity and degree of disruption, loss of banding, degree of collagen packing, fibril size variability and its intrafibrilar oedema, each meniscus was pointed from 0 to 7. Subsequently they were classified in grades ranging from a normal state (grade I; 0 to 2 points) to severe disarray (grade III; 5 to 7 points). RESULTS: The fibril collagen diameters of those menisci that had been previously frozen showed an average size in the longitudinal section of 14.256 nm, whereas 17.279 nm were seen in the menisci used as controls (p=0.019). In the transverse section, the frozen menisci averaged 13.145 nm and 16.935 nm the controls (p=0.003). Samples of the 13 previously frozen menisci were classified as grade III in 8 cases (61,54 %), and grade II in 5 cases (38.46 %). They averaged 4.846 points. The control groups were classified as grade I in 6 cases (46.154%) and grade II in 7 cases (53.85 %). The frozen menisci averaged 4.85 points whereas the control group did so 2.46 (p CONCLUSIONS: The fibril diameters in frozen menisci showed a thinner diameter and had a higher degree of disarray. Therefore, the results suggest that the freezing process alters the menisci’s collagen net. This could partially explain the pathological changes found in shrunken menisci. This is the first work that quantified and qualified methodologically the collagen meniscal architecture and its potential changes.

Freezing causes changes in the menisci collagen net. a new ultrastructural menisci disarray scale.

A 65-year-old man presented with a left medial meniscus (MM) posterior root tear (PRT). Unicompartmental knee arthroplasty was performed 12 months after transtibial pullout repair of the MMPRT. Repaired MM posterior root tissue was subjected to histological analysis. Immunostaining and picrosirius red staining showed sufficient deposition of type I collagen, and hematoxylin-eosin staining using a polarized microscope showed well-aligned fiber orientation in the repaired tissue. The repaired posterior root (post-transtibial pullout repair) showed mature and well-aligned ligament-like tissue. Preserving the MM posterior root remnant to mimic the original posterior root tissue might be useful when performing pullout repair.

Histological Analysis of Repaired Tissue after Pullout Repair of a Medial Meniscus Posterior Root Tear.

Abstract: Hyperphosphatemia is independently linked with vascular calcification, cardiovascular disease, bone-mineral disease, progression of renal insufficiency, and all-cause mortality in chronic kidney disease (CKD) and end-stage renal disease (ESRD). The emerging importance of fibroblast growth factor-23 (FGF-23) and its co-factor Klotho play very important roles as phosphaturic hormones; however, phosphate levels rise due to a loss of renal Klotho production and the phosphaturic effects of the FGF-23/Klotho axis. Hyperphosphatemia is also associated with calciphylaxis, acceleration of renal tubulointerstitial disease, renal osteodystrophy, and uremic cardiomyopathy. This review incorporates ultrastructural remodeling of the thoracic aorta to provide a different perspective on vascular calcification. Nine-week-old male heterozygous (mRen2) 27 (Ren2) rat models of hypertension, insulin resistance, vascular oxidative stress and albuminuria are utilized to demonstrate aortic remodeling associated with vascular calcification. Nine-week-old male Zucker obese (fa/fa) rat models are utilized to better understand nephrolith formation. Phosphate homeostasis, toxicity, multiple metabolic and uremic toxicities, renal osteodystrophy, and vascular calcification are also discussed. Additionally, the role of the endothelium, vascular smooth muscle cells, inflammatory monocytes/macrophages and mast cells, pericytes, oxidative stress, hydrogen sulfide, and extraosseous calcification in the kidney are discussed as they relate to CKD, ESRD and calciphylaxis. 

Phosphate Toxicity and Vascular Calcification in Chronic Kidney Disease: A Closer Look Utilizing Transmission Electron Microscopy.

Background:The collagen ultrastructure of torn medial meniscus posterior roots (MMPRs) has not been precisely defined.Purpose:To investigate the ultrastructure of torn MMPRs, focusing on their coll...

Collagenous Ultrastructure of the Torn Medial Meniscus Posterior Root: A Transmission Electron Microscopy Study:

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Collagenous Ultrastructure of the Torn Medial Meniscus Posterior Root: A Transmission Electron Microscopy Study: