Gold Beads Implantation (GBI) – The Scientific Basis
Dr. Sagiv Ben-Yakir BSc(Biology), DVM(in honor), MRCVS, CVA(IVAS), CVHomotox(Baden-Baden, Germany)
Received: January 2009
Received: January 2009
Noble metals, like gold, have been used since ancient times as cures for a wide range of diseases (1). The use of gold implants was originated from acupuncture where gold needles had been used in the Far East (1).
In the early 1970s some American veterinarians (Dr. Grady Young, followed by Dr. Terry Durkes) started to treat dogs suffering from hip dysplasia with gold implants (2). The implantation was usually done at acupoints GB-29, GB-30, and BL-54, which lie close to the affected hip joint. Other arthritic conditions (e.g. elbow arthrosis, spinal spondylosis etc) had been treated similarly by implanting gold beads in other local acupuncture points chosen accordingly (3). Today, many veterinary acupuncturists around the world implant gold beads, or short lengths of 24-carat gold wire, routinely to treat chronic diseases in animals.
The mechanism of action proposed by proponents of gold beads implantation (GBI) is that the gold implants emit a minute positive electrical charge that neutralizes a negative electrical charge of the point, producing analgesia and preventing further arthritic changes at the joint (2,4).
However, there is another possible explanation for the basic scientific mechanism behind GBI. On insertion of metallic gold beads, in vivo and in situ, it was found that gold ions are released from the implanted gold and diffuse out into the surrounding tissue. This phenomenon mimics on a local scale the treatment with gold-containing drugs used for arthritic conditions (5).
Almost immediately after implantation, local macrophages and other inflammatory cells attach themselves to the metallic gold surfaces (6). This attachment is mediated by activation of the complement system as C3 adsorbs to the implant surface. The C3 forms complexes with complement factor B or factor H resulting in the formation of C3b or iC3B respectively. C3b or iC3B are both ligands for macrophages surface receptors. Additionally, fibronectin and vitronectin also absorb to the locally implanted surface of the gold bead and act as a ligand for the macrophages through RGD-integrin receptor domains. These and other ligand-interactions are the primarily interactions between gold surface and macrophages and other inflammatory cells. The inflammatory cells produce an ultra-thin layer, a dissolution membrane, within which the necessary chemistry for liberation of gold ions is found. This is 10-100 nm thick biolayer membrane essential for the dissolution of metal implants and particles (which cannot be phagocytosed).
The inflammatory cells (e.g. macrophages, other neutrophils) release cyanide into the dissolution membrane and into their immediate surroundings (7,8,9). The following chemical process occurs:
4Au + 8CN- + 2H20 + O2 = 4[Au(CN)2]- + 4OH-
The complex ion aurocynide Au(CN)2- , a relatively stable ion, inhibits the lysosomal enzymes of inflammatory cells in the synovial tissue and decreases the number of inflammatory cells in situ. Also, the aurocynide ions inhibit antigen processing and suppress NF-kappa B-binding activity and I-kappa B-kinase activation, and in turn reduce the production of pro-inflammatory cytokines. Aurocynide is the active substance that inhibits the cellular functions of inflammatory cells (10,11,12).
Also, these ions move from their dissolution membrane location into intercellular space, where they are taken up both by the macrophages and by other inflammatory cells further away.
It was found also that the longer the gold implant stays in the inflamed tissue, the further away gold ions are carried by inflammatory cells. It was also found that when the cells surrounding the gold implant become heavily loaded they leave their position on the dissolution membrane and are replaced by new inflammatory cells (5,6).
In the early 1970s some American veterinarians (Dr. Grady Young, followed by Dr. Terry Durkes) started to treat dogs suffering from hip dysplasia with gold implants (2). The implantation was usually done at acupoints GB-29, GB-30, and BL-54, which lie close to the affected hip joint. Other arthritic conditions (e.g. elbow arthrosis, spinal spondylosis etc) had been treated similarly by implanting gold beads in other local acupuncture points chosen accordingly (3). Today, many veterinary acupuncturists around the world implant gold beads, or short lengths of 24-carat gold wire, routinely to treat chronic diseases in animals.
The mechanism of action proposed by proponents of gold beads implantation (GBI) is that the gold implants emit a minute positive electrical charge that neutralizes a negative electrical charge of the point, producing analgesia and preventing further arthritic changes at the joint (2,4).
However, there is another possible explanation for the basic scientific mechanism behind GBI. On insertion of metallic gold beads, in vivo and in situ, it was found that gold ions are released from the implanted gold and diffuse out into the surrounding tissue. This phenomenon mimics on a local scale the treatment with gold-containing drugs used for arthritic conditions (5).
Almost immediately after implantation, local macrophages and other inflammatory cells attach themselves to the metallic gold surfaces (6). This attachment is mediated by activation of the complement system as C3 adsorbs to the implant surface. The C3 forms complexes with complement factor B or factor H resulting in the formation of C3b or iC3B respectively. C3b or iC3B are both ligands for macrophages surface receptors. Additionally, fibronectin and vitronectin also absorb to the locally implanted surface of the gold bead and act as a ligand for the macrophages through RGD-integrin receptor domains. These and other ligand-interactions are the primarily interactions between gold surface and macrophages and other inflammatory cells. The inflammatory cells produce an ultra-thin layer, a dissolution membrane, within which the necessary chemistry for liberation of gold ions is found. This is 10-100 nm thick biolayer membrane essential for the dissolution of metal implants and particles (which cannot be phagocytosed).
The inflammatory cells (e.g. macrophages, other neutrophils) release cyanide into the dissolution membrane and into their immediate surroundings (7,8,9). The following chemical process occurs:
4Au + 8CN- + 2H20 + O2 = 4[Au(CN)2]- + 4OH-
The complex ion aurocynide Au(CN)2- , a relatively stable ion, inhibits the lysosomal enzymes of inflammatory cells in the synovial tissue and decreases the number of inflammatory cells in situ. Also, the aurocynide ions inhibit antigen processing and suppress NF-kappa B-binding activity and I-kappa B-kinase activation, and in turn reduce the production of pro-inflammatory cytokines. Aurocynide is the active substance that inhibits the cellular functions of inflammatory cells (10,11,12).
Also, these ions move from their dissolution membrane location into intercellular space, where they are taken up both by the macrophages and by other inflammatory cells further away.
It was found also that the longer the gold implant stays in the inflamed tissue, the further away gold ions are carried by inflammatory cells. It was also found that when the cells surrounding the gold implant become heavily loaded they leave their position on the dissolution membrane and are replaced by new inflammatory cells (5,6).
References:
1. “Gold Symposium 1st, June 20, 2007 at Institute of Anatomy, Aarhus University Denmark.
2. “Gold Bead Implants” by Durkes T. E. in “Veterinary Acupuncture, Ancient Art to Modern Medicine” ed. by Schoen A. M. 2nd edition, Mosby, USA, 2001, Chapter 25, pp 303-305.
3. “Gold Bead Implantation” by Durkes T. E. in International Veterinary Acupuncture Society Certification Course notes, San Diego, USA, 1989-1990.
4. “Revolutionary new pain theory and acupuncture treatment procedure based on new theory of acupuncture mechanism” by Takase K, in Am J. Acupuncture 11:305-323, 1983.
5. “In vivo liberation of gold ions from gold implants. Autometallographic tracing of gold in cells adjacent to metallic gold” by Danscher G. in Histochem Cell Biol 117:447-452, 2002.
6. “In vitro liberation of charged gold atoms: autometallographic tracing of gold ions released by macrophages grown on metallic gold surfaces” by Larsen A. Stoltenberg M and Danscher G in Histochem Cell Biol 128:1-6, 2007.
7. “The activation of gold complexes by cyanide produced by polymorphonuclear leukocytes, the formation of aurocynide by myeloperoxidase” by Graham G.G in Biochem Pharmacol 39:1697-1702, 1990.
8. “Serum lysozyme: a potential marker of monocyte/macrophage activity in rheumatoid arthritis” by Torsteindottir I et al in Rheumatology 38:1249-1254, 1999.
9. “Molecular mechanism of action of gold treatment in rheumatoid arthritis: an update” by Burmester GR in Z. Rheumatol 60:167-173, 2001.
10. “Mechanism of action of disease modifying anti-rheumatic agent, gold sodium thiomalate” by Mangalam A. K. in Int Immunopharmacol 1:1165-1172, 2001.
11. “Inhibition of IL-6 and IL-8 induction from cultured rheumatoid synovial fibroblasts by treatment with aurothioglucose” by Yoshida S et al in Int Immuno 11:151-158, 1999.
12. “Inhibition of the DNA-binding activity of NF-kappa by gold compounds in vitro” by Yang J.P. in FEBS Lett 361:89-96, 1995.
1. “Gold Symposium 1st, June 20, 2007 at Institute of Anatomy, Aarhus University Denmark.
2. “Gold Bead Implants” by Durkes T. E. in “Veterinary Acupuncture, Ancient Art to Modern Medicine” ed. by Schoen A. M. 2nd edition, Mosby, USA, 2001, Chapter 25, pp 303-305.
3. “Gold Bead Implantation” by Durkes T. E. in International Veterinary Acupuncture Society Certification Course notes, San Diego, USA, 1989-1990.
4. “Revolutionary new pain theory and acupuncture treatment procedure based on new theory of acupuncture mechanism” by Takase K, in Am J. Acupuncture 11:305-323, 1983.
5. “In vivo liberation of gold ions from gold implants. Autometallographic tracing of gold in cells adjacent to metallic gold” by Danscher G. in Histochem Cell Biol 117:447-452, 2002.
6. “In vitro liberation of charged gold atoms: autometallographic tracing of gold ions released by macrophages grown on metallic gold surfaces” by Larsen A. Stoltenberg M and Danscher G in Histochem Cell Biol 128:1-6, 2007.
7. “The activation of gold complexes by cyanide produced by polymorphonuclear leukocytes, the formation of aurocynide by myeloperoxidase” by Graham G.G in Biochem Pharmacol 39:1697-1702, 1990.
8. “Serum lysozyme: a potential marker of monocyte/macrophage activity in rheumatoid arthritis” by Torsteindottir I et al in Rheumatology 38:1249-1254, 1999.
9. “Molecular mechanism of action of gold treatment in rheumatoid arthritis: an update” by Burmester GR in Z. Rheumatol 60:167-173, 2001.
10. “Mechanism of action of disease modifying anti-rheumatic agent, gold sodium thiomalate” by Mangalam A. K. in Int Immunopharmacol 1:1165-1172, 2001.
11. “Inhibition of IL-6 and IL-8 induction from cultured rheumatoid synovial fibroblasts by treatment with aurothioglucose” by Yoshida S et al in Int Immuno 11:151-158, 1999.
12. “Inhibition of the DNA-binding activity of NF-kappa by gold compounds in vitro” by Yang J.P. in FEBS Lett 361:89-96, 1995.
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