Table 2 Characteristics of in vitro studies about the effect of teriparatide on OA
From: Potential effects of teriparatide (PTH (1–34)) on osteoarthritis: a systematic review
Author (year, country) | Subjects | Intervention | Dose (duration) | Route | Findings |
|---|---|---|---|---|---|
Chang et al. (2009, China) [25] | Human articular chondrocytes | PTH (1–34) | 10 nM (10 days) | Co-culture | PTH (1–34) reverses the progression of terminal differentiation of human articular chondrocytes PTH (1–34) could be used to treat early OA without affecting normal chondrocytes |
Shao et al. (2022, China) [45] | BMSCs | PTH (1–34) | 10 nM (48 h) | Co-culture | PTH (1–34) alleviates OA by increasing the migration, proliferation, and chondral matrix formation of OA chondrocytes by inhibiting proinflammatory cytokines |
Chang et al. (2016, China) [46] | Human articular chondrocyte | PTHrP | 10−8 to 10−7 M (7 days) | Co-culture | PTH (1–34) is beneficial for preventing the chondro-degenerative changes initiated by dexamethasone treatment |
Mwale et al. (2010, Canada) [47] | Human MSCs | PTH (1–34) | 100 nM (48 h) | Co-culture | p38 and AKT protein kinase signaling pathways may not be required to initiate the regulation of expression of COLII and COLX by PTH (1–34), which is necessary for preventing precocious MSC hypertrophy |
Funk et al. (1998, USA) [48] | RA and OA synovial tissue | PTHrP (1–40)/PTHrP (60–72)/PTHrP (1–86) | 0.3 pM (24 h) | Co-culture | Proinflammatory cytokine-stimulated production of NH2 terminal PTHrP by synovial tissue directly invading cartilage and bone in RA, which might mediate joint destruction through direct effects on cartilage or indirectly via the induction of mediators of bone resorption |
Petersson et al. (2006, Sweden) [49] | RA or OA Chondrocytes | PTHrP (1–34) | 0.1 to 100 nM (15 days) | Co-culture | PTHrP (1–34) increases proliferation of human chondrocytes PTHrP (1–34) increases the amount of YKL-40 from chondrocytes derived from RA patients |
Music et al. (2020, Australia) [50] | BMSCs | PTH (1–34) | 0, 1, 10, or 100 nM (14 days) | Co-culture | PTH (1–34) suppresses BMSC hypertrophic gene expression in chondrogenic cultures PTH (1–34) has an anti-hypertrophic effect and a catabolic effect on BMSC as they become increasingly differentiated |
Tsukazaki et al. (1996, Japan) [51] | Human chondrocytes | PTH (l–34)/hPTHrP (l–141)/hPTHrP (100–114) | 10−13 to 10−7 M (120 min) | Co-culture | PTHrP is thought to be an important autocrine/paracrine factor for chondrocyte metabolism No significant difference of exogenously PTHrP (1–141) regard to the action of these agents, cell growth, differentiation |
Dogaki et al. (2016, Japan) [52] | Hematoma-derived progenitor cells | PTH (1–34) | 100 nM (14 days) | Co-culture | Pulsatile PTH (1–34) works on human cartilages in regarding to proliferation, osteogenic, and chondrogenic differentiation PTH (1–34) administration after fracture might positively act on other cells that contribute to fracture healing |
Hosokawa et al. (2015, Japan) [53] | ATDC5 cells | PTH (1–34) | 10−10/10−9/10−8 M (21 days) | Co-culture | PTH (1–34) regulates ATDC5 cells in both chondrogenesis and the circadian clock as time-dependent properties of chondrocyte function and differentiation |
Rutgers et al. (2019, Netherlands) [54] | Human chondrocytes | PTH (1–34) | 0.1 or 1.0 μM (4 weeks) | Co-culture | PTH (1–34) inhibits healthy human articular chondrocytes regeneration other than hypertrophic differentiation PTH (1–34) may be suitable for cartilage repair based on MSCs |