Ehlers-Danlos syndrome (EDS) was first described over 100 years ago, and is now recognized more often with many subgroups of classification. EDS is considered genetic-related hereditary connective-tissue disorder. Common symptoms include hypermobile loose joints, joint pain, stretchy velvety skin, and is associated with cardio-vascular problems including aortic dissection, joint subluxation and dislocation, scoliosis, chronic pain, and a multitude of growing list of symptoms. Is it possible that EDS is the final manifestation of reprogrammed host DNA or epigenome by bacterial pathogens? By the way, Hippocrates described “excessive mobility” in 400 B.C and hypermobile joints are old news, but naming Ehlers-Danlos syndrome (EDS) is new.
Recently I saw a young woman with vague chest pain and hypermobile joints. She was told she had cardiovascular related Ehlers-Danlos syndrome (EDS) by an EDS specialist from the east coast. My evaluation indicated she had hidden dental infections in old wisdom teeth extraction sites based on acupuncture meridian assessment (AMA) that was affecting her vague chest pain. Her dental X-rays were normal. I sent her to an oral surgeon to clean out the old infected dental jaw socket areas and her vague chest pain was resolved. I also sent her to see a rheumatologist for a second opinion for EDS and the rheumatologist told her she did not have EDS. This case makes you think about overdiagnosing Ehlers-Danlos syndrome, possibly from mimicking EDS-like symptoms from other factors.
Hidden dental infections are one of the most common denominators for mimicking hundreds of medical diagnoses. Common problems include chronic fatigue, arthritis, fibromyalgia and chronic pain, cardiovascular problems including chest pain and stroke, kidney problems, autoimmune disorders, neurologic disorders, and many unknown symptoms including EDS from my personal clinical observations. Several patients I have seen for other medical problems also had EDS as a part of their medical history, and they also had hidden dental and parasite infections.
Currently, EDS is considered a genetic disorder that occurs due to variations of more than 19 genes that are present and defects in the structure or processing of the protein collagen. Diagnosis is often based on symptoms and genetic testing or skin biopsy. There is no cure since EDS is considered a genetic disorder. Treatment is supportive therapy including physical therapy and braces to support the joints and muscles.
As of 2017, there were 13 subtypes of EDS classified based on certain diagnostic criteria:
Hypermobile EDS
Classical EDS
Vascular EDS
Kyphoscoliosis EDS
Arthrochalasia EDS
Dermatosparaxis EDS
Brittle Cornea syndrome
Classical-like EDS
Spondylodysplastic EDS
Musculocontractural EDS
Myopathic EDS
Periodontal EDS
Cardiac-valvular EDS
As I saw the young woman with EDS-like symptoms resolve after dental work, I began to explore the connections between hidden dental infections and EDS with limited information. EDS may make you more susceptible to periodontal infection, but not the other way around. Periodontal involvement may lead to the diagnosis of underlying systemic EDS condition, but there is no literature supporting that dental-periodontal infection might be the culprit of EDS. Periodontal EDS is a rare disorder characterized by soft, hyperextensible skin, abnormal scarring, easy bruising and generalized periodontitis with early loss of teeth. Is it possible that some unrecognized infections may trigger genetic expressions and we assume that the EDS is solely a genetic inherited disorder?
I came across a 2014 article by Silmon and Kim in The American Journal of Pathology titled, Pathogens Hijack the Epigenome: A New Twist on Host-Pathogen Interactions. They state, “Pathogens have evolved strategies to promote their survival by dramatically modifying the transcriptional profile and protein content of the host cell they infect. Modifications of the host transcriptome and proteome are mediated by pathogen-encoded effector molecules that modulate host cells through a variety of different mechanisms… Host gene regulatory mechanisms may be targeted through cytoplasmic signaling, directly by pathogen effector proteins, and possibly by pathogen RNA.”
A 2018 case report by Mozayeni et al. in Medicine indicated systemic Bartonella infection associated joint hypermobility mimicking EDS, type III and to consider systemic bartonellosis as a differential diagnosis for EDS. Modulation of host signaling pathways, targeting host nuclear proteins, post-translational modification and molecular mimicry of nuclear proteins by pathogens and immortalization and oncogenesis, etc. are a part of biohacking of epigenomes that we are beginning to accept with some limited understanding.
Here is a case (not an Ehlers-Danlos syndrome case) of a chronic fatigue, fibromyalgia patient with a multitude of symptoms. She was referred for cavitation surgery. The DNA ConneXions test results of her dental biopsy indicated many hidden dental infections. In my experience, dental problems are often a driving force for inflammation, in effect biohacking epigenomes into many different medical diagnoses.
In summary, hypermobile joints have been around for many years but the actual diagnosis of Ehlers-Danlos syndrome (EDS) has been only recently recognized with many subclassifications based on individual symptoms. Many medical specialists are managing their patients’ unique symptoms with support therapies. There is no cure for EDS. However, some chronic disease patients with EDS symptoms that have been treated for other underlying risk factors – such as dental infections or Bartonella, parasites or fungal infections – have their EDS symptoms improve. Treat the underlying infections and it might modify the expression of epigenomes and stop the biohacking. For me, a treatment plan is based on acupuncture meridian assessment (AMA) and balancing the meridians, not based on medical diagnosis. For EDS, Lyme, or chronically ill patients, hidden dental infections and parasites are the most often neglected medical conundrum.
