Concurrent treatment of oral and systemic maladies using direct current electricity

A method and apparatus to the concurrent treatment of multiple oral diseases and defects while boosting overall oral hygiene utilizing electricity are supplied for non-human animals. Electrodes are used to provide an electrical current into the gingival tissues of a mouth so as to attain a number of therapeutic, prophylactic, and medicinal advantages. These benefits comprise killing oral microbes, increasing oral vasodilation, reducing oral biofilm, improving oral blood circulation, reversing oral bone resorption, promoting oral osteogenesis, treating gum recession, and fostering regeneration. Other benefits include the treatment of gingivitis, periodontitis, and oral malodor, and other systemic diseases correlated with oral pathogens.

 

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BACKGROUND

 

 
This invention relates to an apparatus configured to simultaneously promote general oral hygiene, cure periodontal diseases such as gingivitis and periodontitis, kill oral microbes such as cavity-causing bacteria, reduce oral biofilms, increaseblood flow in oral tissues, increase salivation, encourage gingival tissue regeneration, foster osteogenesis in the boney structures of the teeth, mouth and related areas, treating systemic diseases related to oral bacteria, also cure otherperiodontal and oral maladies throughout the noninvasive use of weak direct current electricity into the membranes in the oral cavity, and it also relates to an apparatus acceptable for supplying direct current electricity for these therapeutic,prophylactic, and regenerative effects.
 

 
Periodontal disease has been identified as a risk factor for various systemic diseases from both physicians and physicians. Contained in such ailments are cardiovascular disease, adverse pregnancy outcomes, and diabetes with newfound evidencesupporting its association with pancreatic diseases and arthritis. Though many of the studies demonstrate correlation between the presence of periodontal disease and such systemic conditions, causation, with the majority of these conditions, is still a subject ofongoing research. Some of the biological mechanisms which have been suggested as to how oral bacteria stemming from periodontal disease can cause systemic illness are as followed:
 

 
1. Immediate result of oral infections: mucous membranes and their byproducts can gain systemic gain through the circulatory system via traveling through compromised tissue and inflamed periodontium from the nasal cavity. In gaining systemic accessibility,oral microbes have the capacity to directly affect subclinical mediators of various systemic diseases.
 

 
2. Illness: Individuals with periodontal disease have elevated levels of systemic inflammatory markers on account of the burden of increased amounts of bacteria. Treatment for periodontal disease has been reported to decrease systemicinflammation levels.
 

 
3. Cross-reactivity: The progression of systemic disorders can be accelerated from the immune reaction to bacterial heat-shock proteins creating antibodies that cross-react with inborn heat shock proteins extracted cells of the damaged tissues.
 

 

Cardiovascular Disease

 

 
Studies investigating the possible association between periodontal disease and cardiovascular diseases, including atherosclerosis, coronary heart disease, and stroke have found a substantial positive correlation between poor oral health and theprevalence of cardiovascular disease. While the two diseases share several common risk factors, recent studies indicate that periodontitis can clot and therefore contribute to atherosclerotic complications. In fact, meta-analyses reveal that subjectssuffering from periodontitis experience an increased risk for developing cardiovascular ailments.
 

 
While it has not been shown if those bacteria initiate atherosclerosis or instead invade an already compromised artery, antibodies to periodontal bacteria, such as Fuseobacterium nucleatum and Streptococcus oralis, have been foundin blood clots and are associated with an increased risk of coronary heart disease. A mouse study found that intravenous inoculation with Porphyromonas gingivalis accelerated atherosclerotic development. Further, after oral inoculation, P.gingivalis DNA was found in the tissue of those infected mice which showed visible indications of accelerated early atherosclerosis. Another study has called F. nucleatum as a synergistic agent with P. gingivalis. F. nucleatum enhances the ability ofP. Gingivalis to invade host cells due to a coaggregating effect between both organisms. This is important as germs inside the atheroma can lead to the development of atherosclerotic plaque. The evidence thus far supports the thought thatperiodontitis contributes to systemic exposure to oral bacteria that serves as a potential source of systemic inflammatory mediators, cytokines produced from the infected periodontal tissues, capable of initiating or worsening atherosclerosis and coronary heartdisease when they enter into the blood stream. Clinical studies on periodontal disease also have demonstrated a positive association with coronary artery disease and emphasis is now being placed on understanding the exact connection between periodontal disease andatherosclerosis.
 

 

Pre-term Birth

 

 
Fusobaceterium nucleatum, one of the most common species of bacteria found in amniotic fluid and placental infections that cause preterm birth, can be often named the sole infectious agent in preterm labour with intact fetal membranes. F.nucleatum is also highly associated with various kinds of periodontal disease. During periodontal disease, once the oral mucosa is inflamed and infected and the amounts of periodontal pathogens increase radically, transient levels of germs canappear from the blood leading to selective colonization of undesirable sites. 1 study revealed that pregnant mice injected hematogenously with F. nucleatum isolated from either amniotic fluid disease or an oral supply led to fetal death.
 

 
Recently, an individual stillbirth situation was analyzed and it was found that the F. nucleatum did indeed originate from the mother’s oral cavity, a truth that had not yet been demonstrated. It is very likely that the F. nucleatum translocated from the mother’smouth via the blood stream where it was then able to cross the endothelium to proliferate and colonize inside the fetal membranes, amniotic fluid and plaques whereupon its existence contribute to fetal demise. In a mouse model, hematogenous injection of F.nucleatum to pregnant mice led to specific bacterial colonization from the placenta causing localized inflammation. F. nucleatum was totally removed from the maternal circulation after 24 hours of injection. However, once colonized in theimmune privileged placenta, the germs proliferated quickly and induced fetal death in 3 days. Chronic periodontal disease could mediate infection through the translocation of periodontal bacteria/inflammatory markers into the fetoplacental unit.
 

 

Diabetes

 

 
Diabetes mellitus is an endocrine disease that stems from genetic, behavioral and environmental risk factors. For the past several decades, diabetes has been regarded as a changing factor for periodontal disease with recent decades suggesting abidirectional connection between them both. Further, the presence of periodontal disease has been implicated as a risk for diabetic complications, specifically poor glycemic control. Recent longitudinal and systemic studies have observed periodontal diseasecorrelated to higher risks of death from ischemic heart disease, diabetic nephropathy, end-stage renal disease and increased insulin resistance compared to patients with mild or no periodontal disease. In type II diabetes, insulin resistance is linkedto the activities of pro-inflammatory cytokines. It’s thought that periodontal disease leads to a significantly higher volume of these serum markers of inflammation, thus conferring insulin resistance. A human study analyzing the bacterial content ofadults with and without type II diabetes found diabetic patients had significantly more severe periodontitis and higher degrees of many oral bacteria, such as Streptococcus oralis.
 

 

Pyogenic Liver Abscess

 

 
F. nucleatum has recently been implicated in pyogenic liver abscess (PLA). Normally caused by biliary tract pathology, diverticular disease and bowel malignancy, atrophic gastritis and cryptogenic liver disorder, PLA caused by F. nucleatum isvery rare with Escherichia coli, Klebsiella and Enterobacter being the most commonly isolated microorganisms in the drained abscesses. F. nucleatum was found at the liver abscess without any additional infectious origin being found, except for a dentalextraction. It’s hypothesized that due to this coaggregation properties of F. nucleatum, it can transfer and breach the mucosa of the colon and lead to bacteremia which leads to hepatic abscess.
 

 

Osteomyelitis

 

 
Osteomyelitis is a bone infection caused by bacteria, fungi or other germs. Usually, bacteria spreads to the bone from infected skin, muscles or tendons and frequently time happen under a skin sore. The infection can also start in another part ofthe body and spread hematogenously. Sometimes Fusobacterium species are isolated from bone/joint infections in the head and throat region and have been correlated with chronic periodontitis. A recent study has reported a case of osteomyelitis caused byF. Nucleatum in combination with muscle abscess. The patient had no known predisposing factors and had no other infection sources except a record of periodontal disease. It is thought that due to the patient’s poor oral hygiene, F. nucleatumbacteremia may have developed and lead to some hematogenous osteomyelitis of the lower leg.
 

 

Arthritis

 

 
Several clinical studies have suggested a possible association between rheumatoid arthritis (RA) and periodontal disease as several oral bacteria species, such as P. gingivalis and Prevotella intermedia, have been isolated from your synovialfluid of patients. Periodontal disease is thought to allow bacteria to penetrate through the permeable pocket epithelial in the oral cavity to reach the inherent gingival connection tissue. From that point, it may be transported out into the bloodstreamwith the capability to colonize elsewhere inside the body. The oral bacteria found in the synovial fluid of patients suffering from RA was credited to synovial inflammation favorably trapping oral bacteria DNA, which suggests periodontal disease mayhave a perpetuating effect on joint diseases. Therefore, periodontitis can in reality be a factor resulting in the autoimmune inflammatory responses feature of RA. Patients suffering from RA may also be at a higher risk of developing periodontaldisease hence suggesting a bidirectional relationship between both conditions. One specific study analyzed the presence of bacterial DNA in the synovial fluids of indigenous and failed prosthetic joints of patients suffering from arthritis. Out of the5 patients in which bacterial DNA was found, F. nucleatum was detected in 4 of these 5 patients. This suggests that this bacterium may translocate from the nasal cavity to the synovial fluid, as F. nucleatum was additionally found in the patient’s plaque sample.
 

 

Oral Biofilm

 

 
Periodontitis, gingivitis, and caries are infectious diseases of the oral cavity where oral biofilm plays a significant role. Biofilm formation is also involved in the pathogenesis of dental implant failures such as peri-implantitis, denturestomatitis, and oral yeast infections such as candidiasis. Oral biofilms begin with dental pellicle formation on tooth. This pellicle consists of salivary proteins that coat the exposed surfaces of your teeth, mainly the supra-gingival ones,into which the planktonic bacteria begin to adhere. The aerobic bacteria, including gram-positive cocci, such as S. oralis, are the early colonizers that begin forming the initial biofilm colony, primarily through cellular branch of the adherentbacteria.
 

 
When the first colony has been established, other co-aggregating bacteria species, for example F. nucleatum, P. gingivalis, and other gram-negative, anaerobic bacteria attach to the formerly formed colonies. As these colonies grow, they growto cover the sub-gingival surfaces of their teeth and begin to cause inflammation in the periodontium.
 

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