Abstract
PurposeOsteoarthritis (OA) is a prevalent, progressively degenerative disease. Researchers have rigorously documented clinical improvement in participants receiving prolotherapy for OA. The mechanism of action is unknown; therefore, basic science studies are required. One hypothesized mechanism is that prolotherapy stimulates tissue proliferation, including that of cartilage. Accordingly, this in vitro study examines whether the prolotherapy agent phenol-glycerin-glucose (P2G) is associated with upregulation of proliferation-enhancing cytokines, primarily fibroblast growth factor-2 (FGF-2).MethodsMurine MC3T3-E1 cells were cultured in a nonconfluent state to retain an undifferentiated osteochondroprogenic status. A limitation of MC3T3-E1 cells is that they do not fully reproduce primary human chondrocyte phenotypes; however, they are useful for modeling cartilage regeneration in vitro due to their greater phenotypic stability than primary cells. Two experiments were conducted: one in duplicate and one in triplicate. Treatment consisted of phenol-glycerin-glucose (P2G, final concentration of 1.5%). The results were assessed by quantitative Reverse Transcriptase-Polymerase Chain Reaction (qRT-PCR) to detect mRNA expression of the FGF-2, IGF-1, CCND-1 (Cyclin-D), TGF-β1, AKT, STAT1, and BMP2 genes.ResultsP2G - treated preosteoblasts expressed higher levels of FGF-2 than water controls (hour 24, p < 0.001; hour 30, p < 0.05; hour 38, p < 0.01). Additionally, CCND-1 upregulation was observed (p < 0.05), possibly as a cellular response to FGF-2 upregulation.ConclusionsThe prolotherapy agent P2G appears to be associated with upregulation of the cartilage cell proliferation enhancer cytokine FGF-2, suggesting an independent effect of P2G consistent with clinical evidence. Further study investigating the effect of prolotherapy agents on cellular proliferation and cartilage regeneration is warranted.
Highlights
Osteoarthritis (OA) is a common, impactful and progressively degenerative disease [8, 14, 46] characterized by cartilage erosion that leads to degradation of joint structure and function [9, 22]
The prolotherapy agent P2G appears to be associated with upregulation of the cartilage cell proliferation enhancer cytokine fibroblast growth factor-2 (FGF-2), suggesting an independent effect of P2G consistent with clinical evidence
Further study investigating the effect of prolotherapy agents on cellular proliferation and cartilage regeneration is warranted
Summary
Osteoarthritis (OA) is a common, impactful and progressively degenerative disease [8, 14, 46] characterized by cartilage erosion that leads to degradation of joint structure and function [9, 22]. The development of therapy that stimulates cartilage regeneration and controls pain is the subject of active research. Clinical data [50] and recent clinical trials and meta-analysis data [53] support reduced pain and stiffness and improved function in patients undergoing this treatment. Physician scientists hypothesize a multifactorial mechanism of action [51], with one specific hypothesis positing that prolotherapy slows OA progression by stimulating cartilage regeneration [31]. This hypothesis is supported by a study of 6 OA patients that used pre- and postarthroscopic imaging and histological staining to show clinical evidence suggesting that HD stimulates joints to regrow cartilage [55]
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