+ Site Statistics
+ Search Articles
+ Subscribe to Site Feeds
EurekaMag Most Shared ContentMost Shared
EurekaMag PDF Full Text ContentPDF Full Text
+ PDF Full Text
Request PDF Full TextRequest PDF Full Text
+ Follow Us
Follow on FacebookFollow on Facebook
Follow on TwitterFollow on Twitter
Follow on LinkedInFollow on LinkedIn

+ Translate

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

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

International Journal of General Medicine 6(): 277-290

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. 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. 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. 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. 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. 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.

(PDF emailed within 0-6 h: $19.90)

Accession: 055333224

Download citation: RISBibTeXText

PMID: 23637551

DOI: 10.2147/IJGM.S43852

Related references

Chemokine RANTES/CCL5 as an unknown link between wound healing in the jawbone and systemic disease: is prediction and tailored treatments in the horizon?. Epma Journal 6(1): 10-10, 2015

Immunohistochemical localization of growth factors fibroblast growth factor-1 and fibroblast growth factor-2 and receptors fibroblast growth factor receptor-2 and fibroblast growth factor receptor-3 in normal oral epithelium, epithelial dysplasias, and squamous cell carcinoma. Oral Surgery Oral Medicine Oral Pathology Oral Radiology & Endodontics 93(5): 573-579, 2002

Follow-up of patients with systemic immunological diseases undergoing fatty-degenerative osteolysis of the jawbone surgery and treated with RANTES 27CH. Journal of Biological Regulators and Homeostatic Agents 32(1): 37-45, 2018

Recruitment of Matrix Metalloproteinase-9 (MMP-9) to the Fibroblast Cell Surface by Lysyl Hydroxylase 3 (LH3) Triggers Transforming Growth Factor-β (TGF-β) Activation and Fibroblast Differentiation. Journal of Biological Chemistry 290(22): 13763-13778, 2015

Increased expression of transforming growth factor-beta1, acidic fibroblast growth factor, and basic fibroblast growth factor in fetal versus adult fibroblast cell lines. Laryngoscope 110(4): 616-619, 2000

Expression of transforming growth factor-alpha/epidermal growth factor receptor, hepatocyte growth factor/c-met, acidic fibroblast growth factor/fibroblast growth factor receptors during hepatocarcinogenesis. Hepatology 18(4 PART 2): 160A, 1993

Expression of transforming growth factor alpha/epidermal growth factor receptor, hepatocyte growth factor/c-met and acidic fibroblast growth factor/fibroblast growth factor receptors during hepatocarcinogenesis. Carcinogenesis 17(5): 931-938, 1996

Importance of vascular phenotype by basic fibroblast growth factor, and influence of the angiogenic factors basic fibroblast growth factor/fibroblast growth factor receptor-1 and ephrin-A1/EphA2 on melanoma progression. American Journal of Pathology 160(3): 1009-1019, 2002

Epidermal growth factor, transforming growth factor alpha, transforming growth factor beta, acidic fibroblast growth factor, basic fibroblast growth factor, and interleukin-1 proteins in the cornea. Experimental Eye Research 59(1): 63-71, 1994

Localization of acidic fibroblast growth factor, fibroblast growth factor receptor-4, transforming growth factor-alpha, and epidermal growth factor receptor in human endocrine cells of the gut and related tumors: An immunohistochemical study. Applied Immunohistochemistry 6(4): 199-208, 1998

Involvement of basic fibroblast growth factor in fibroblast-stimulatory serum activity of a patient with systemic lupus erythematosus and multiple dermatofibromas. Dermatology 191(4): 281-285, 1995

The suppression of fibroblast growth factor 2/fibroblast growth factor 4-dependent tumour angiogenesis and growth by the anti-growth factor activity of dextran derivative (CMDB7). British Journal of Cancer 78(1): 111-118, 1998

Stable and temperature-sensitive transformation of rat kidney epithelial cells suppresses expression of acidic fibroblast growth factor 1 but activates secretion of fibroblast growth factor 3 (int-2) and vascular endothelial growth factor. Cell Growth & Differentiation 5(4): 349-357, 1994

Constitutive expression of an intracellular form of fibroblast growth factor receptor triggers myogenic differentiation. Journal of the American College of Cardiology 0(SPEC ISSUE): 292A, 1995

Vascular endothelial growth factor a heparin binding growth factor with a different distribution than basic fibroblast growth factor in normal brain and alzheimers disease. Society for Neuroscience Abstracts 17(1-2): 196, 1991