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

Identifieur interne : 002E32 ( Pmc/Curation ); précédent : 002E31; suivant : 002E33

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

Auteurs : Johann Lechner [Allemagne] ; Volker Von Baehr [Allemagne]

Source :

RBID : PMC:3636973

Abstract

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.


Url:
DOI: 10.2147/IJGM.S43852
PubMed: 23637551
PubMed Central: 3636973

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PMC:3636973

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<title>Background</title>
<p>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.</p>
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<title>Objectives</title>
<p>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.</p>
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<title>Materials and methods</title>
<p>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.</p>
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<title>Results</title>
<p>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.</p>
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<title>Discussion</title>
<p>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.</p>
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<p>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.</p>
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<pmc article-type="research-article">
<pmc-dir>properties open_access</pmc-dir>
<front>
<journal-meta>
<journal-id journal-id-type="nlm-ta">Int J Gen Med</journal-id>
<journal-id journal-id-type="iso-abbrev">Int J Gen Med</journal-id>
<journal-title-group>
<journal-title>International Journal of General Medicine</journal-title>
</journal-title-group>
<issn pub-type="epub">1178-7074</issn>
<publisher>
<publisher-name>Dove Medical Press</publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id pub-id-type="pmid">23637551</article-id>
<article-id pub-id-type="pmc">3636973</article-id>
<article-id pub-id-type="doi">10.2147/IJGM.S43852</article-id>
<article-id pub-id-type="publisher-id">ijgm-6-277</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Original Research</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>RANTES and fibroblast growth factor 2 in jawbone cavitations: triggers for systemic disease?</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Lechner</surname>
<given-names>Johann</given-names>
</name>
<xref ref-type="aff" rid="af1-ijgm-6-277">1</xref>
<xref ref-type="corresp" rid="c1-ijgm-6-277"></xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>von Baehr</surname>
<given-names>Volker</given-names>
</name>
<xref ref-type="aff" rid="af2-ijgm-6-277">2</xref>
</contrib>
</contrib-group>
<aff id="af1-ijgm-6-277">
<label>1</label>
Clinic for Integrative Dentistry, Munich, Germany</aff>
<aff id="af2-ijgm-6-277">
<label>2</label>
Compartment of Immunology and Allergology on Institute for Medical Diagnostics in MVZ GbR, Berlin, Germany</aff>
<author-notes>
<corresp id="c1-ijgm-6-277">Correspondence: Johann Lechner, Clinic for Integrative Dentistry, Gruenwalder Str 10A, 81547 Munich, Germany Tel +49 89 697 00 55 Fax +49 89 692 58 30 Email
<email>drlechner@aol.com</email>
</corresp>
</author-notes>
<pub-date pub-type="collection">
<year>2013</year>
</pub-date>
<pub-date pub-type="epub">
<day>22</day>
<month>4</month>
<year>2013</year>
</pub-date>
<volume>6</volume>
<fpage>277</fpage>
<lpage>290</lpage>
<permissions>
<copyright-statement>© 2013 Lechner and von Baehr, publisher and licensee Dove Medical Press Ltd</copyright-statement>
<copyright-year>2013</copyright-year>
<license>
<license-p>This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.</license-p>
</license>
</permissions>
<abstract>
<sec>
<title>Background</title>
<p>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.</p>
</sec>
<sec>
<title>Objectives</title>
<p>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.</p>
</sec>
<sec>
<title>Materials and methods</title>
<p>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.</p>
</sec>
<sec>
<title>Results</title>
<p>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.</p>
</sec>
<sec>
<title>Discussion</title>
<p>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.</p>
</sec>
<sec>
<title>Conclusion</title>
<p>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.</p>
</sec>
</abstract>
<abstract abstract-type="graphical">
<title>Video abstract</title>
<p>
<media xlink:href="IJGM-6-277-s.avi" xlink:type="simple" id="d35e116" position="anchor" mimetype="video" mime-subtype="x-msvideo"></media>
</p>
</abstract>
<kwd-group>
<title>Keywords</title>
<kwd>RANTES</kwd>
<kwd>CCL5</kwd>
<kwd>fibroblast growth factor</kwd>
<kwd>FGF-2</kwd>
<kwd>bead-based Luminex analysis</kwd>
<kwd>osteolytic degenerated jaw bone</kwd>
<kwd>NICO</kwd>
<kwd>systemic signaling pathways</kwd>
</kwd-group>
</article-meta>
</front>
<floats-group>
<fig id="f1-ijgm-6-277" position="float">
<label>Figure 1</label>
<caption>
<p>NICO sample completely converted to fatty spongial marrow of the jawbone.</p>
<p>
<bold>Abbreviation:</bold>
NICO, neuralgia-inducing cavitational osteonecrosis.</p>
</caption>
<graphic xlink:href="ijgm-6-277Fig1"></graphic>
</fig>
<fig id="f2-ijgm-6-277" position="float">
<label>Figure 2</label>
<caption>
<p>Microscopic view of NICO sample completely converted to fatty spongial marrow of the jawbone.</p>
<p>
<bold>Abbreviation:</bold>
NICO, neuralgia-inducing cavitational osteonecrosis.</p>
</caption>
<graphic xlink:href="ijgm-6-277Fig2"></graphic>
</fig>
<fig id="f3-ijgm-6-277" position="float">
<label>Figure 3</label>
<caption>
<p>Pathohistological structure of typical NICO tissue.</p>
<p>
<bold>Abbreviation:</bold>
NICO, neuralgia-inducing cavitational osteonecrosis.</p>
</caption>
<graphic xlink:href="ijgm-6-277Fig3"></graphic>
</fig>
<fig id="f4-ijgm-6-277" position="float">
<label>Figure 4</label>
<caption>
<p>Bead-based processing of NICO samples.</p>
</caption>
<graphic xlink:href="ijgm-6-277Fig4"></graphic>
</fig>
<fig id="f5-ijgm-6-277" position="float">
<label>Figure 5</label>
<caption>
<p>Distribution of seven cytokines in NICO (n = 31) and in normal jawbone (n = 3) (values in pg/mL).</p>
<p>
<bold>Abbreviations:</bold>
FGF-2, fibroblast growth factor 2; IL, interleukin; MCP-1, monocyte chemotactic protein 1; NICO, neuralgia-inducing cavitational osteonecrosis; ra, receptor antagonist; RANTES, regulated upon activation normal T-cell expressed and secreted/chemokine ligand 5; TNF, tumor necrosis factor.</p>
</caption>
<graphic xlink:href="ijgm-6-277Fig5"></graphic>
</fig>
<fig id="f6-ijgm-6-277" position="float">
<label>Figure 6</label>
<caption>
<p>RANTES in NICO tissue with cohort assigned to diseases.</p>
<p>
<bold>Abbreviations:</bold>
ALS, amyotrophic lateral sclerosis; CFS, chronic fatigue syndrome; MaCa, breast cancer; MS, multiple sclerosis; neuro-Deg, neurodegenerative disease; NICO, neuralgia-inducing cavitational osteonecrosis; RANTES, regulated upon activation, normal T-cell expressed, and secreted/chemokine ligand 5; Rheuma, rheumatoid arthritis.</p>
</caption>
<graphic xlink:href="ijgm-6-277Fig6"></graphic>
</fig>
<fig id="f7-ijgm-6-277" position="float">
<label>Figure 7</label>
<caption>
<p>Assignment of FGF-2 levels (pg/mL) in 31 NICO samples to diseases.</p>
<p>
<bold>Abbreviations:</bold>
ALS, amyotrophic lateral sclerosis; CFS, chronic fatigue syndrome; FGF-2, fibroblast growth factor 2; MaCa, breast cancer; MS, multiple sclerosis; Neuro-Deg, neurodegenerative disease; NICO, neuralgia-inducing cavitational osteonecrosis; RANTES, regulated upon activation, normal T-cell expressed, and secreted/chemokine ligand 5; Rheuma, rheumatoid arthritis.</p>
</caption>
<graphic xlink:href="ijgm-6-277Fig7"></graphic>
</fig>
<fig id="f8-ijgm-6-277" position="float">
<label>Figure 8</label>
<caption>
<p>RANTES levels in pathological tissues and mean difference compared to RANTES expression in the NICO cohort.</p>
<p>
<bold>Abbreviations:</bold>
CervCa, cervical cancer; lit, data from literature; MaCa, breast cancer; NICO, neuralgia-inducing cavitational osteonecrosis; RANTES, regulated upon activation, normal T-cell expressed, and secreted/chemokine ligand 5; RheumArthr, rheumatoid arthritis.</p>
</caption>
<graphic xlink:href="ijgm-6-277Fig8"></graphic>
</fig>
<fig id="f9-ijgm-6-277" position="float">
<label>Figure 9</label>
<caption>
<p>FGF-2 levels in pathological tissues and mean difference compared to FGF-2 expression in the NICO cohort.</p>
<p>
<bold>Abbreviations:</bold>
FGF-2, fibroblast growth factor 2; lit, data from literature; MaCa, breast cancer; Ma tissue no find, breast tissue no pathological findings; MS, multiple sclerosis; NICO, neuralgia-inducing cavitational osteonecrosis; ProstCa, prostate cancer.</p>
</caption>
<graphic xlink:href="ijgm-6-277Fig9"></graphic>
</fig>
<fig id="f10-ijgm-6-277" position="float">
<label>Figure 10</label>
<caption>
<p>Comparison of RANTES and FGF-2 expression (pg/mL) in BC tissues and in NICO in five BC patients.</p>
<p>
<bold>Abbreviations:</bold>
BC, breast cancer; FGF-2, fibroblast growth factor 2; lit, literature; MaCa o.B., ; MaCa, breast cancer; NICO, neuralgia-inducing cavitational osteonecrosis; RANTES, regulated upon activation, normal T-cell expressed, and secreted/chemokine ligand 5.</p>
</caption>
<graphic xlink:href="ijgm-6-277Fig10"></graphic>
</fig>
<fig id="f11-ijgm-6-277" position="float">
<label>Figure 11</label>
<caption>
<p>Comparison of RANTES/FGF-2 (pg/mL) in synovial fluid in RA and in NICO in four RA patients.</p>
<p>
<bold>Abbreviations:</bold>
FGF-2, fibroblast growth factor 2; lit, data from literature; NICO, neuralgia-inducing cavitational osteonecrosis; RANTES, regulated upon activation, normal T-cell expressed, and secreted/chemokine ligand 5; RA/Rheuma, rheumatoid arthritis; Prost tissue, prostate tissue with no pathological findings; Ma tissue, breast tissue with no pathological findings.</p>
</caption>
<graphic xlink:href="ijgm-6-277Fig11"></graphic>
</fig>
<fig id="f12-ijgm-6-277" position="float">
<label>Figure 12</label>
<caption>
<p>Comparison of FGF-2 levels in serum/CFS/control from literature with FGF-2 levels in NICO in one patient with ALS and two patients with MS.</p>
<p>
<bold>Abbreviations:</bold>
ALS, amyotrophic lateral sclerosis; CSF, cerebrospinal fluid; FGF-2, fibroblast growth factor-2; lit, data from literature; MS, multiple sclerosis; NICO, neuralgia-inducing cavitational osteonecrosis; Pat, patient with.</p>
</caption>
<graphic xlink:href="ijgm-6-277Fig12"></graphic>
</fig>
</floats-group>
</pmc>
</record>

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HfdIndexSelect -h $EXPLOR_AREA/Data/Pmc/Curation/RBID.i   -Sk "pubmed:23637551" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/Pmc/Curation/biblio.hfd   \
       | NlmPubMed2Wicri -a EdenteV2 

Wicri

This area was generated with Dilib version V0.6.32.
Data generation: Thu Nov 30 15:26:48 2017. Site generation: Tue Mar 8 16:36:20 2022