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RANTES and fibroblast growth factor 2 in jawbone cavitations: triggers for systemic disease?

Authors Lechner J, von Baehr V

Received 9 February 2013

Accepted for publication 7 March 2013

Published 22 April 2013 Volume 2013:6 Pages 277—290

DOI https://doi.org/10.2147/IJGM.S43852

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 4

Video abstract presented by Johann Lechner

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Johann Lechner,1 Volker von Baehr2

1Clinic for Integrative Dentistry, Munich, Germany; 2Compartment of Immunology and Allergology on Institute for Medical Diagnostics in MVZ GbR, Berlin, Germany

Background: Jawbone cavitations (JC) are hollow dead spaces in jawbones with dying or dead bone marrow. These areas are defined as fatty degenerative osteonecrosis of the jawbone or neuralgia-inducing cavitational osteonecrosis and may produce facial pain. These afflictions have been linked to the immune system and chronic illnesses. Surgical debridement of JC is reported to lead to an improvement in immunological complaints, such as rheumatic, allergic, and other inflammatory diseases (ID). Little is known about the underlying cause/effect relationship.
Objectives: JC bone samples were analyzed to assess the expression and quantification of immune modulators that can play a role in the pathogenesis of IDs. The study supports a potential mechanism where JC is a mediating link in IDs.
Materials and methods: Samples of fatty softened bone taken from JCs were extracted from 31 patients. The specimens were analyzed by bead-based multiplex technology and tested for seven immune messengers.
Results: Regulated upon activation, normal T-cell expressed, and secreted (RANTES) and fibroblast growth factor (FGF)-2 were found at high levels in the JCs tested. Other cytokines could not be detected at excessive levels.
Discussion: The study confirms that JC is able to produce inflammatory messengers, primarily RANTES, and, secondarily, FGF-2. Both are implicated in many serious illnesses. The excessive levels of RANTES/FGF-2 in JC patients with amyotrophic lateral sclerosis, multiple sclerosis, rheumatoid arthritis, and breast cancer are compared to levels published in medical journals. Levels detected in JCs are higher than in the serum and cerebrospinal fluid of amyotrophic lateral sclerosis and multiple sclerosis patients and four-fold higher than in breast cancer tissue.
Conclusion: This study suggests that JC might serve as a fundamental cause of IDs, through RANTES/FGF-2 production. Thus, JC and implicated immune messengers represent an integrative aspect of IDs and serve as a possible cause. Removing JCs may be a key to reversing IDs. There is a need to raise awareness about JC throughout medicine and dentistry.

Keywords: RANTES/CCL5, fibroblast growth factor, FGF-2, bead-based Luminex analysis, osteolytic degenerated jaw bone, NICO, systemic signaling pathways

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