Action Mechanisms of Small Extracellular Vesicles in Inflammaging.

The accumulation process of proinflammatory components in the body due to aging influences intercellular communication and is known as inflammaging. This biological mechanism relates the development of inflammation to the aging process. Recently, it has been reported that small extracellular vesicles (sEVs) are mediators in the transmission of paracrine senescence involved in inflammatory aging. For this reason, their components, as well as mechanisms of action of sEVs, are relevant to develop a new therapy called senodrugs (senolytics and senomorphic) that regulates the intercellular communication of inflammaging. In this review, we include the most recent and relevant studies on the role of sEVs in the inflammatory aging process and in age-related diseases such as cancer and type 2 diabetes.

Human Cartilage Engineering in an In Vitro Repair Model Using Collagen Scaffolds and Mesenchymal Stromal Cells.

The purpose of this study was to investigate cartilage repair of in vitro lesion models using human bone marrow mesenchymal stromal cells (hBMSCs) with different collagen (Col) scaffolds. Lesions were made in human cartilage biopsies. Injured samples were pre-treated with interleukin 1ß (IL1ß) for 24 h; also, samples were not pre-treated. hBMSCs were seeded on different types of collagen scaffolds. The resulting constructs were placed into the lesions, and the biopsies were cultured for 2 months in chondrogenic medium. Using the modified ICRSII scale, neotissues from the different scaffolds showed ICRS II overall assessment scores ranging from 50% (fibrocartilage) to 100% (hyaline cartilage), except for the Col I +Col II +HS constructs (fibrocartilage/hyaline cartilage, 73%). Data showed that hBMSCs cultured only on Col I +Col II +HS scaffolds displayed a chondrocyte-like morphology and cartilage-like matrix close to native cartilage. Furthermore, IL1ß pre-treated biopsies decreased capacity for repair by hBMSCs and decreased levels of chondrogenic phenotype of human cartilage lesions.

Myofascial Release Therapy in the Treatment of Occupational Mechanical Neck Pain: A Randomized Parallel Group Study.

OBJECTIVE: As myofascial release therapy is currently under development, the objective of this study was to compare the effectiveness of myofascial release therapy with manual therapy for treating occupational mechanical neck pain. DESIGN: A randomized, single-blind parallel group study was developed. The sample (n = 59) was divided into GI, treated with manual therapy, and GII, treated with myofascial release therapy. Variables studied were intensity of neck pain, cervical disability, quality of life, craniovertebral angle, and ranges of cervical motion. RESULTS: At five sessions, clinical significance was observed in both groups for all the variables studied, except for flexion in GI. At this time point, an intergroup statistical difference was observed, which showed that GII had better craniovertebral angle (P = 0.014), flexion (P = 0.021), extension (P = 0.003), right side bending (P = 0.001), and right rotation (P = 0.031). A comparative analysis between therapies after intervention showed statistical differences indicating that GII had better craniovertebral angle (P = 0.000), right (P = 0.000) and left (P = 0.009) side bending, right (P = 0.024) and left (P = 0.046) rotations, and quality of life. CONCLUSIONS: The treatment of occupational mechanical neck pain by myofascial release therapy seems to be more effective than manual therapy for correcting the advanced position of the head, recovering range of motion in side bending and rotation, and improving quality of life.

Quantification of cells expressing mesenchymal stem cell markers in healthy and osteoarthritic synovial membranes.

OBJECTIVE: To quantify cells expressing mesenchymal stem cell (MSC) markers in synovial membranes from human osteoarthritic (OA) and healthy joints. METHODS: Synovial membranes from OA and healthy joints were digested with collagenase and the isolated cells were cultured. Synovial membrane-derived cells were phenotypically characterized for differentiation experiments using flow cytometry to detect the expression of mesenchymal markers (CD29, CD44, CD73, CD90, CD105, CD117, CD166, and STRO-1) and hematopoietic markers (CD34 and CD45). Chondrogenesis was assessed by staining for proteoglycans and collagen type II, adipogenesis by using a stain for lipids, and osteogenesis by detecting calcium deposits. Coexpression of CD44, CD73, CD90, and CD105 was determined using immunofluorescence. RESULTS: Cells expressing MSC markers were diffusely distributed in OA synovial membranes; in healthy synovial membrane these cells were localized in the subintimal zone. More numerous MSC markers in OA synovial membranes were observed in cells also expressing the CD90 antigen. FACS analysis showed that more than 90% of OA synovial membrane-derived cells were positive for CD44, CD73, and CD90, and negative for CD34 and CD45. OA synovial membrane-derived cells were also positive for CD29 (85.23%), CD117 (72.35%), CD105 (45.5%), and STRO-1 (49.46%). Micropellet analyses showed that the culture of cells with transforming growth factor-ß3 stimulated proteoglycan and collagen type II synthesis. CONCLUSION: Synovial membranes from patients with OA contain more cells positive for CD44, CD90, and CD105 antigens than those from joints with undamaged cartilage.