Actinomycotic Oral Infection (Modern Dental Implants and Root Canals)

Corresponding Author: R.S. Carlson, Inventor of the Carlson Bridge®,Honolulu, Hawai, USA. Email: ddscarlson@hawaiiantel.net Citation: R.S. Carlson. Actinomycotic Oral Infection (Modern Dental Implants and Root Canals). Int J Dent & Oral Heal. 3:8, 82-96 DOI: 10.25141/2471-657X-2017-8.0069 Copyright: ©2017 R.S. Carlson. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited


Introduction ISSN 2471-657X
If one were to inspect the general research regarding the effectiveness and physiological acceptability and safety of the modern dental implant tooth replacement, one is met with a "mixed bag of information" on their real success rates, systemic biological impacts, and advisability as a method of single or multiple tooth replacement. For example, reported in various credible peer reviewed journals for the years 2016 and 2017 we see that, contrary to the touted 98% success rate asserted about by the implant manufacturers, it is widely held that "success" can vary from about 91 % to 49% over a three to five year period or longer depending on the opinion of the clinical observer(s). The main issue that has been identified for implant degradation and ultimate re-treatment or removal of the implant is PI-"Peri-Implantits" Charalampakis et al, in their paper of 2013 from Gothenburg titled Periimplantitis from a microbiological perspective, stated it precisely: "Thus, the prospect of reaching a consensus (regarding PI) is continuously hampered and the magnitude of the incidence of peri-implantitis still remains therefore a matter of academic dispute." Charalampakis et al continue "Any factor proposed to be a risk factor for…peri-implantitis should not just be an extract of a statistical significant result in a paper but relate to the disease with biological plausibility." We would like to present biological plausibility not only relating to the implant post or fixtures locally but to the oral systemic biota-the total human. We are not "academics" but clinical scientists. We shall not enter discussions of the "life-span" of implants, their functionality, their being the so-called "golden standard" of our tooth replacement in our profession-prosthetic dentistry-but we shall offer a brief clinical scientific review of our observations and research. The first biological factor is that of microbial infection within the soft tissues and bone about the dental implant. The second biological factor is that of the direct currents (DC electrical currents) generated by the implant fixtures, post, abutment, and replacement crown. Let us explore both of these factors that fulfill the parameter of biological plausibility in the ensuing conversation and be open to our further exploration.

Actinomyces and Actinomycosis
I the early 1980s we began to remove infected root canal teeth and associated soft tissue and bone (Odonton) and send them for pathological inspection by a board certified histopathologist. The findings were remarkably revealing to this date.
In brief all of the 349 "odontons" inspected it was found that acute-chronic inflammation-sometimes marked, reactive bone, dead bone, osteomyelitis, granuloma, cyst, abscess and other attending abnormalities were present in the jaw below the tooth in question. Having carried this root canal research on since about 1983, we have also extended this methodology to implant removal due to infections or otherwise.
Background on factors causing "marked acute-chronic inflammation." As we know the dead tooth has no circulatory system internally-in a sense this is the definition of an endodontically treated tooth. As the dead tooth degrades it gives off various chemicals such as putresciene, cadaverine, thioethers, and what we call "endo-toxins." This fact is no longer disputed in the scientific clinical profession, not in academia either.
Another factor for inflammation is bacterial presence in tissues where they should not be. As a habit in the early days of our research the pathologist noted what he called "star-like microganisms" in colonies with rays in the bone and soft tissues. He noted that they were certainly colonies of actinomyces that surrounded the root canal. However, it must be understood that we had not asked for a determination of bacterial review, it was an incidental finding in his pathology reports to me.
Actinomyces in know from the 1800s as the "ray fungus," mistaken as a fungus until about 1938. It is currently identified a bacterium: Actinomyces is a genus of the Actinobacteria class of bacteria. They are all gram positive. Actinomyces species are facultatively anaerobic and they grow best under anaerobic con-R.S. Carlson. Actinomycotic Oral Infection (Modern Dental Implants and Root Canals). Int J Dent & Oral Heal. 3:8, 82-96 DOI:10.25141/2471-657X-2017 ditions. Actinomyces species may form endospores, and, while individual bacteria are rodshaped, Actinomyces colonies form fungus-like branched networks of hyphe. They are implicated in decay and gum or perio disease in the oral cavity since normal residents. However, it is not normal to find actinomyces in bone or connective tissues deep in the other jawbone or in the blood vascular system. If found in the jaw bone it may lead to a condition known as "luppy jaw"-an abscess from either dental or peri-dental origins, or both. Systemically it may lead to Actinomycosis a condition where abscesses occur-through circulatory migration or facial migration-into jaw, throat, lungs, abdomen, genital areas.
Actinobacteria are normally present in the gums and are the most common cause of infection in dental procedures and oral abscesses. Many Actinomyces species are opportunistic pathogens of humans and other mammals, particularly in the oral cavity. In rare cases, these bacteria can cause actinomycosis, a disease characterized by the formation of abscesses in the mouth, lungs, or the gastrointestinal tract. Actinomycosis is most frequently caused by A Israeli, which may also cause endocarditis, though the resulting symptoms may be similar to those resulting from infections by other bacterial species. Aggreatibacter actinomycetemcomitans has been identified as being of note in periodontal disease.
The genus is typically the cause oral-cervicofacial disease. It is characterized by a painless "lumpy jaw". Lymphadenopathy is uncommon in this form of the disease. Another form of actinomycosis is thoracic disease, which is often misdiagnosed as a neoplasm, as it forms a mass that extends to the chest wall. It arises from aspiration of organisms from the oropharynx. Symptoms include chest pain, fever, and weight loss. Abdominal disease is another manifestation of actinomycosis. This can lead to a sinus tract that drains to the abdominal wall or the perianal area. Symptoms include fever, abdominal pain, and weight loss. Some Actinomyces species have also been shown to infect the nervous system of some animals without apparent trauma. The bacteria Actinomyces are ubiquitous and abundant in soil. They are known for the important role they play in soil ecology; they produce a number of enzymes that help degrade plant root debris and waste materials. Thus their presence is important in the formation of compost. They are also known for causing diseases in humans and livestock, usually when they get an opportunity to gain access to the body's interior through wounds. As with other opportunistic infections, people with immunologic issues are at higher risk. In all of the preceding traits and in their branching filament formation, they bear similarities to Norcardia causing Norcardosis a similar illness as Actinomycosis.
It is well established that actinomycosis is an endogenous infec-tion. The causative Actinomyces species reside on mucosal surfaces and gain access to deeper tissues via trauma, surgical procedures, or foreign bodies, which disrupt the mucosal barrier. Inside the tissue, these bacteria form masses consisting of aggregates of branching, filamentous bacilli. Actinomycosis is defined as a hard mass-type lesion with a specific histopathological structure. There are a large number of case reports of actinomycosis in the literature, but in most cases, diagnosis has been based solely on clinical and histopathological findings. In the majority of early reports, microbiological confirmation of diagnosis was lacking. Even when microbiological assessment was included, culture was typically the only method used. If, however, antimicrobial treatment had been started before sample collection, the results of culture may be falsely negative. The increasing introduction of molecular bacterial detection and identification methods is helping to overcome such problems.
An internal abscess is more difficult to identify, but signs include pain in the affected area, a high temperature, and generally feeling unwell. Internal abscesses rarely heal themselves, so prompt medical attention is indicated if such an abscess is suspected. This is important in the resolution of infected abscessed teeth, that they be surgically removed and bone cleansing-cavitation-accomplished.

Dental Implant Associated Mircro Currents
Rarely mentioned in any research in this day is the impact of direct currents on the tissues around the metal implant-corrosion impact. The human cellular structures operate electrically in all actions in pico-ampers, 10-12 amperers. Tiller related in Vibrational Medicine by Gerbber1987 that currents greater than pico-amps (in the direction of nano-amps 10-9 and micro-amps 10-6) will cause cell destruction while currents smaller than pico-amps stimulate cellular growth. In our measurements of this phenomenon in titanium implants we have recorded amps -36 uA (uA = micro-amps) and even higher-over -100uA-when the coupled anode and cathode is to gold crowns, metal bridges, metal partials and amalgam fillings. This is an area ripe for investigation for both titanium and zirconia dental implants. Galvanic impacts on human tissues are well known but little studied. In the removal of infected and problematic dental implants we have found also the deleterious impact associated with deep dental structures beyond the post above the gum, deep in the bone crypt. Again, we have over the past 17 years removed various dental implants (about 30) in 20 patients and sent them to the histopathologist at Queen's Hospital Honolulu, Hawai'i. We present the data of both the "root canal teeth" study and the "implants" study in two tables. The first table will show implants alone and the second all teeth and implants removed since 1986. R.S. Carlson. Actinomycotic Oral Infection (Modern Dental Implants and Root Canals). Int J Dent & Oral Heal. 3:8, 82-96 DOI:10.25141/2471-657X-2017 Table1. Dental Implants 19 patients with 30 implants 10 of the 19 had (50%) Actinomyces, infectingattachment tissues (bone-ligaments).
R.S. Carlson. Actinomycotic Oral Infection (Modern Dental Implants and Root Canals). Int J Dent & Oral Heal. 3:8, 82-96 DOI:10.25141/2471-657X-2017 Histo-Patholoical Studies 1986-2017 of Soft Tissue & Bone About The Roots of Endo Teeth and Metal Implants Done at Queens Hospital Honolulu, Hawaii Table 2. Endo Teeth and Dental Implants R.S. Carlson. Actinomycotic Oral Infection (Modern Dental Implants and Root Canals). Int J Dent & Oral Heal. 3:8, 82-96 DOI:10.25141/2471-657X-2017 R.S. Carlson. Actinomycotic Oral Infection (Modern Dental Implants and Root Canals). Int J Dent & Oral Heal. 3:8, 82-96 DOI:10.25141/2471-657X-2017 Conclusion It is commonplace in this year 2017 to read in our dental journals and hear our media extoll the modern advancements of dental implants as being the natural replacement for the failed root canal tooth. It seems that we go from the frying pan to the fire in this regard. As our two tables reveal the microbiologic factor from both are the presence of actinomyces; and, the mirco-currents from dental metals in these oral tissues that may not only play a significant role in failures of implants and root canals but may migrate to other parts of the human biome and play their mischief. We as biological dental practitioners caution the misuse of these two methods, root canals or dental implants, for treatment particularly in our youth and seniors who may have compromised immunity.
As Charalampakis notes in his presentation referenced at the start of our inquiry: "It is common knowledge that mircroorganisims are a risk factor for peri-implantitis since disease is bacterially induced... Unfortunately the bacterial role is disease pathogenesis has been underrated because no specific bacteria have been implicated in the apical migration of the 'barrier' epithelium, equivalent to the junctional epithelium around teeth." We might now humbly suggest that there may be a specific bacterium present and is prevalent in the oral environment with significant virulence whose primary function in nature is the reclamation of dead and dying matter, including the human biome. Due to the microbiological difficulty of showing actinomyces odontolyticus or any of its family members in peri-implant tissue through testing methods in the lab, we may have a subclinical factor revealed by R.S. Carlson. Actinomycotic Oral Infection (Modern Dental Implants and Root Canals). Int J Dent & Oral Heal. 3:8, 82-96 DOI:10.25141/2471-657X-2017 this clinical research as presented. We have shown that in over 50% of the implants removed and histologically inspected that colonies of actinomyces were present associated with the pathological picture. One may not conclude that actinomyces alone is a causative agent but that, perhaps, they are one of the elements to be investigated more comprehensively. The second equally unknown factor not looked at much at all is the implication of electrical currents in tissue surrounding metal dental implants, their corrosion products/toxins. Given the fact that body cells operate on pico-amps in normal states and that the currents generated by metal implants are in the micro-amps range, about three fold higher, this fact may give pause to our understanding of cellular destruction due to corrosion (acid base balance) and the need for immune cell phagocytosis and bacterial phagocytosis in the deep surrounding tissues of implants.
Dr. RS Carlson graduated from the University of Michigan School of Dentistry in 1969 and completed Post Graduate training in pediatric dentistry with Strong-Carter Dental Clinic, Honolulu, Hawaii, 1970-71. He is a founder of Kokua Kalihi Valley Dental Clinic in 1973 (http://www.kkv.net/index.php/history) and volunteered from 1973 to 1980 serving low-income families and immigrant populations from the South Pacific Islands and Asia. He has maintained a private practice in Honolulu since 1971 emphasizing Bio-Logical Dentistry. He can be reached at (808) 735-0282, ddscarlson@hawaiiantel.net or carlsonbiologicaldentistry.com. Disclosure: Dr. Carlson is the inventor of the Carlson Bridge® "Winged Pontic" tooth replacement system, a noninvasive approach to replacing missing teeth, with patents issued in November 1999 and October 2001.