Condition Focus: Bone Remodeling — Osteoblast-Osteoclast Balance
Bone is not a static structure — it is constantly being remodeled through the coordinated activity of osteoblasts (which build new bone) and osteoclasts (which break down old bone). In healthy joints, this process is balanced. In chronic gout, the balance shifts toward resorption: inflammatory cytokines from repeated flares activate osteoclasts while suppressing osteoblast activity, leading to periarticular bone erosion visible on X-rays.
This study from Hong and colleagues used an innovative co-culture system — growing osteoblasts and osteoclasts together in the same dish — to test how PBM affects bone remodeling when both cell types can communicate through paracrine signalling. The key finding: 808 nm PBM at 1.2 J/cm² enhanced osteoblast differentiation while simultaneously reducing osteoclast differentiation.
The mechanism was mediated through the RANKL/OPG axis — the master regulatory system for bone remodeling. RANKL (receptor activator of NF-κB ligand) promotes osteoclast formation and activity. OPG (osteoprotegerin) acts as a decoy receptor that blocks RANKL. PBM decreased RANKL and increased OPG, shifting the balance firmly toward bone protection.
Critically, this dual effect was only observed in the co-culture system, not when each cell type was cultured alone. This means PBM’s bone-protective effect depends on the cell-cell communication that occurs in actual bone tissue — making the co-culture model more clinically relevant than isolated cell experiments.
G.O.A.T. for Gout Alignment:
The G.O.A.T.’s 850 nm wavelength is close to the 808 nm used in this study. The RANKL↓/OPG↑ shift demonstrated here directly addresses the bone erosion pathway activated by chronic gout inflammation. For patients with radiographic evidence of periarticular erosion, the G.O.A.T. may support bone-protective remodeling alongside its anti-inflammatory effects.
Link to original research here
Editor’s note: The cell-type specific dose-response for bone cells is further detailed in Na et al 2018. The comprehensive bone repair review with parameter tables is provided by Lu et al 2024. For the broader connective tissue context including bone, cartilage, and tendon, see Houreld et al 2022. The RANKL/NF-κB connection links to the anti-inflammatory NF-κB suppression reviewed in Immunomodulatory Effects 2025.
Related Articles
- Dose Analysis of PBM on Osteoblast, Osteoclast, and Osteocyte – Na et al 2018
- The Role of PBM in Accelerating Bone Repair – Lu et al 2024
- PBM, Cells of Connective Tissue and Repair – Houreld et al 2022
- Immunomodulatory Effects of PBM: Comprehensive Review – 2025
- PBM in Proliferation/Differentiation of Stem Cells – Miranda et al 2020
Key Takeaways
- PBM enhances osteoblast differentiation while suppressing osteoclast activity — simultaneously
- RANKL↓/OPG↑ shift — the master bone-protective mechanism
- Effect only seen in co-culture — requires cell-cell communication, more clinically relevant
- 808 nm at 1.2 J/cm² — close to G.O.A.T.’s 850 nm wavelength
Study Overview
| Study Type: | In vitro (osteoblast-osteoclast co-culture) |
| Wavelength(s): | 808 nm Ga-Al-As laser |
| Treatment Protocol: | 1.2 J/cm²; co-culture system |
| Sample Size: | Co-culture + isolated cell groups |
| Primary Outcome: | Osteoblast differentiation↑; osteoclast activity↓; RANKL↓/OPG↑ |
Full Citation
Hong JU, et al. (2022). Photobiomodulation effects on bone remodeling in osteoblast and osteoclast co-culture. Lasers in Medical Science, 37, 243–253. View Publication
