The Potential of Menstrual Blood-Derived Mesenchymal Stem Cells for Cartilage Repair and Regeneration: Novel Aspects.

Menstrual blood is a unique body fluid that contains mesenchymal stem cells (MSCs). These cells have attracted a great deal of attention due to their exceptional advantages including easy access and frequently accessible sample source and no need for complex ethical and surgical interventions, as compared to other tissues. Menstrual blood-derived MSCs possess all the major stem cell properties and even have a greater proliferation and differentiation potential as compared to bone marrow-derived MSCs, making them a perspective tool in a further clinical practice. Although the potential of menstrual blood stem cells to differentiate into a large variety of tissue cells has been studied in many studies, their chondrogenic properties have not been extensively explored and investigated. Articular cartilage is susceptible to traumas and degenerative diseases, such as osteoarthritis, and has poor self-regeneration capacity and therefore requires more effective therapeutic technique. MSCs seem promising candidates for cartilage regeneration; however, no clinically effective stem cell-based repair method has yet emerged. This chapter focuses on studies in the field of menstrual blood-derived MSCs and their chondrogenic differentiation potential and suitability for application in cartilage regeneration. Although a very limited number of studies have been made in this field thus far, these cells might emerge as an efficient and easily accessible source of multipotent cells for cartilage engineering and cell-based chondroprotective therapy.

Human articular chondrocytes with higher aldehyde dehydrogenase activity have stronger expression of COL2A1 and SOX9.

OBJECTIVE: To determine in human articular chondrocytes the activity of Aldehyde dehydrogenase (ALDH), which are reported as stem/progenitor cell marker in various adult tissues and evaluate gene expression of ALDH1A isoforms. DESIGN: ALDH activity was evaluated by flow cytometry with Aldefluor™ assay in cells, isolated from human osteoarthritic (OA) cartilage. Its coexpression with surface markers was identified. Cells were sorted according to ALDH activity, and gene expression in sorted populations (ALDH(+) and ALDH(-)) was analyzed by RTq-PCR with Taqman(®) assay. RESULTS: About 40% of freshly isolated chondrocytes demonstrated ALDH activity that remarkably declined during monolayer culture. Markers CD54 and CD55 were significantly stronger expressed, while CD47, CD140b, CD146 and CD166 were depleted in ALDH-expressing (ALDH(pos)) cells. Gene expression analysis revealed significantly higher expression of chondrocyte-specific genes COL2A1, SOX9 and SERPINA1 and lower expression of osteogenic markers RUNX2 and osteocalcin (BGLAP) in sorted ALDH(+) fraction. COL1A1, ACAN, ALPL and stem cell markers NANOG, OCT4, SOX2 and ABCG2 did not differ remarkably between the populations. Genes of isoenzymes ALDH1A2, ALDH1A3 and ALDH2 were strongly expressed, while ALDH1A1 was weakly expressed in chondrocytes. Only ALDH1A2 and ALDH1A3 were significantly enriched in ALDH(+) fraction. CONCLUSIONS: We identified ALDH activity with significantly stronger expression of CD54 and CD55 in human articular chondrocytes. Gene expression of isotypes ALDH1A2, ALDH1A3 and ALDH2 was identified. Coexpression of ALDH activity with chondrogenic markers suggests its association with collagen II producing chondrocyte phenotype. Isotypes ALDH1A2 and ALDH1A3 can be associated with the ALDH activity in these cells.

Recurrent tonsillitis and tonsillectomy in juvenile idiopathic arthritis.

OBJECTIVES: To compare the clinical and bacteriological features of recurrent tonsillitis between patients with and without juvenile idiopathic arthritis (JIA). METHODS: A total of 122 participants, aged 2-18 years, were consecutively recruited into four groups: (i) JIA and recurrent tonsillitis; (ii) JIA; (iii) recurrent tonsillitis; and (iv) healthy. All the patients with recurrent tonsillitis underwent tonsillectomy. Swabs from tonsillar surface crypts of all children and samples from tonsillar core tissue in case of tonsillectomy were processed for culturing. Mycoplasma pneumoniae was determined by polymerase chain reaction (PCR). RESULTS: Significantly lower rates of recurrences but more frequent tonsillar detritus, paratonsillar scars, and more intensive bleeding during tonsillectomy were found in patients with JIA and recurrent tonsillitis, versus patients with recurrent tonsillitis without arthritis. In JIA patients with recurrent tonsillitis, Staphylococcus aureus was cultured from the tonsillar surface in 36%, and from the core tissue in 92% of cases (p = 0.0000). In patients suffering from recurrent tonsillitis alone, this pathogen was cultured from the core in 55.9% of cases (p = 0.0066 compared to JIA patients with recurrent tonsillitis). No M. pneumoniae was revealed by PCR in samples from the tonsillar surface and the core tissue. CONCLUSIONS: The increased rate of S. aureus in the core tissue of tonsils, the higher frequency of tonsillar detritus, the more pronounced paratonsillar scarring, and more intensive bleeding during tonsillectomy, associated with the lower frequency of tonsillitis recurrences, are characteristic for recurrent tonsillitis in JIA as compared to recurrent tonsillitis without arthritis.

New insights into bacterial persistence in reactive arthritis.

Persistence of arthritis-triggering bacteria can cause chronization of reactive arthritis (ReA). In the evaluation of bacterial persistence in ReA, the persistence of both the triggering bacteria and also of the other bacteria residing in the foci of chronic infection, are important. Two forms of bacterial persistence, cell wall-deficient bacteria (L-forms) and bacterial biofilms, are characterized, and the possible links between these forms and ReA are revealed. Data showing the possibility of bacterial ReA triggers to enter the cell wall-deficient state and to persist in bacterial biofilms, and evidence, suggesting that cell wall-deficient bacteria and bacterial biofilms are involved in the foci of chronic infection, are discussed. The understanding of the properties of microbes when they exist in cell wall-deficient state and bacterial biofilms may expand our knowledge on the clinical value of persisting microorganisms in ReA. In conclusion, both modes of persistence, cell wall-deficient state of bacteria and bacterial biofilms, deserve rheumatologists' attention, as their investigation, applying modern standardized methods, may contribute to the elaboration of new beneficial schemes of antibacterial ReA therapy.