Health Effects of Dental Infections and Root-canaled Teeth.

Prestigious dental researchers and doctors such as Westin Price(DDS), Frank Billings (MD), Milton Rosenow (MD) , Charles Mayo(MD) and Martin Fischer(MD) during the early part of the past century based on extensive research concluded that a large portion of chronic systemic disease is due to infections in the tonsils and/or teeth that are usually symptomless and very difficult to detect (25,28-32).

Recently there has been renewed interest in the incidence and effects of oral focal infections. It has been recognized, that oral infection especially periodontitis can cause and affect the course of a number of systemic diseases, such as: cardiovascular disease, cerebrovascular disease, atheromatous peripheral vascular disease, bacterial pneumonia, diabetes mellitus, osteoporosis, and adverse pregnancy outcome (2,29-31). Studies found that treatment of dental infections could bring significant improvement in insulin resistance and other conditions(2bc,29-31).

A significant association has been demonstrated between periodontal disease or other dental related infections and cardiovascular disease (3 a-k,29). Recent studies have demonstrated systemic antibodies to selected periodontal pathogens (3a). A recent study analyzed the prevalence of dental treatment and oral infections related to the development of infective endocarditis (IE)(3b). A retrospective study of 103 cases of IE diagnosed from 1997 to 1999 was conducted in Galicia, Spain. According to the Duke's endocarditis criteria (1994), 87 cases (84.5%) were considered definite IE. A presumed oral portal of entry was recorded in 12 patients (13.7%). Oral infections were held responsible in six cases while the remaining six had received dental treatment in the previous three months (three tooth extractions, one scaling, one cleaning, one fillings). In eight cases of IE, typical oral pathogenic microflora was identified, with Streptococcus viridans being the most frequent. In four of these patients no previous cardiac disease was recorded. The need for increased oral hygiene and improved dental care should be emphasized on preventing IE of dental origin. 

Chronic dental infections, even of low intensity, may cause the development of atherosclerotic changes in arteries, that lead to coronary heart disease(3c). There are many risk factors for atherosclerosis, but the most important are endothelium function disturbances, platelets activation and oxidative changes of plasmatic lipoproteins. Among factors that can induce the epithelium lesions bacterial factor may play an important role. In consequence of the bacterial cell breakdown place the release of endotoxins takes, that lead directly to the damage of endothelial cells. Apart from this direct effect endotoxins activate the fagocytes releasing superoxide reactive radicals, that cause lesions of endothelium. Probably the most widespread chronic bacterial infections in human are the diseases of periodontium and teeth and their inflammatory complications. Oral cavity is colonized by 300-400 bacterial species. In the case of dental bacterial infections bacteriemia occurs after such procedures as tooth extraction, endodontic treatment, therapeutic and hygienic interventions on periodontal tissues. The results of many investigations show the relationship between the oral status (dental and periodontal diseases as chronic oral infections) and disorders of cardiovascular system(3c).

Metabolic syndrome and type 2 diabetes (T2DM) resulting from sustained hyperglycemia are considered as risk factors for cardiovascular disease (CVD) but the mechanism for their contribution to cardiopathogenesis has not been well understood(3def,29). Hyperglycemia induces nonenzymatic glycation of protein-yielding advanced glycationend products (AGE), which are postulated to stimulate interleukin-6 (IL-6) expression, triggering the liver to secrete tissue necrosis factor alpha (TNF-alpha) and C-reactive protein (CRP) that contribute to CVD pathogenesis. Although the high prevalence of periodontitis among individuals with diabetes is well known by dental researchers, it is relatively unrecognized in the medical community. The expression of the same proinflammatory mediators implicated in hyperglycemia (i.e., IL-6, TNF-alpha, and CRP) have been reported to be associated with periodontal disease and increased risk for CVD.

Ford et al (3d) review the evidence for the interaction of oral disease (more specifically, periodontal infections) with cardiovascular disease. Cardiovascular disease is a major cause of death worldwide, with atherosclerosis as the underlying aetiology in the vast majority of cases. The importance of the role of infection and inflammation in atherosclerosis is now widely accepted, and there has been increasing awareness that immune responses are central to atherogenesis. Chronic inflammatory periodontal diseases are among the most common chronic infections, and a number of studies have shown an association between periodontal disease and an increased risk of stroke and coronary heart disease. Although it is recognized that large-scale intervention studies are required, pathogenic mechanism studies are nevertheless required so as to establish the biological rationale. In this context, a number of hypotheses have been put forward; these include common susceptibility, inflammation via increased circulating cytokines and inflammatory mediators, direct infection of the blood vessels, and the possibility of cross-reactivity or molecular mimicry between bacterial and self-antigens. In this latter hypothesis, the progression of atherosclerosis can be explained in terms of the immune response to bacterial heat shock proteins (HSPs). Because the immune system may not be able to differentiate between self-HSP and bacterial HSP, an immune response generated by the host directed at pathogenic HSP may result in an autoimmune response to similar sequences in the host. Furthermore, endothelial cells express HSPs in atherosclerosis, and cross-reactive T cells exist in the arteries and peripheral blood of patients with atherosclerosis. It was concluded that although atherosclerotic cardiovascular disease is almost certainly a multifactorial disease, there is now strong evidence that infection and inflammation are important risk factors. As the oral cavity is one potential source of infection, it is wise to try to ensure that any oral disease is minimized. This may be of significant benefit to cardiovascular health and enables members of the oral health team to contribute to their patients' general health(3d). 

The main deficit in the majority of the studies on the relation of periodontal disease to cardiovascular conditions has been the inadequate control of numerous confounding factors, and the imprecise measurement of the predictor or overadjustment of the confounding variables, resulting in underestimation of the risks(3f,29,31). A meta-analysis of prospective and retrospective follow-up studies has shown that periodontal disease may increase the risk of CVD by approximately 20% (95% confidence interval [CI], 1.08-1.32). Similarly, the reported risk ratio between periodontal disease and stroke is even stronger, varying from 2.85 (CI 1.78-4.56) to 1.74 (CI 1.08-2.81). The association between peripheral vascular disease and oral health parameters has been explored in only two studies, and the resultant relative risks among individuals with periodontitis were 1.41 (CI 1.12-1.77) and 2.27 (CI 1.32-3.90), respectively. Overall, it appears that periodontal disease may indeed contribute to the pathogenesis of cardiovascular disease. 

Thrombotic thrombocytopenic purpura (TTP) is a rare haematological disease of unknown aetiology. This thrombotic microangiopathy is characterized by microvascular lesions with platelet aggregation. It is found in adults and can be associated with pregnancy, cancer, autoimmune diseases, bone marrow transplantation, drugs and bacterial as well as viral infections. The therapy requires a multi-disciplinary team approach involving dentistry. Even if TTP is immediately treated in an adequate manner, it still shows a mortality of up to 20% (3g).  To define a specific treatment concept for periodontal disease and decayed teeth in patients suffering from TTP based on the experiences gained from two cases.  The two patient cases revealed a possible association of TTP with dental foci. Because of the severity and mortality of this disease, both prognosis evaluation and treatment standards of periodontologically compromised or decayed teeth have to be strictly followed in patients suffering from TTP. In order to avoid recurrence of TTP, it seems important to remove radically teeth of questionable prognosis(3g).

The term periodontal medicine encompasses the study of the contribution of periodontal infections on several systemic conditions such as atherosclerosis, myocardial infarction, stroke, diabetes, and premature delivery. The early reports of a linkage between periodontitis and systemic conditions are gaining further support from additional epidemiological studies. The evidence continues to suggest that maternal periodontitis may be an important risk factor or risk indicator for pregnancies culminating in preterm low birth-weight deliveries. Potential mechanisms by which infectious challenge of periodontal origin and systemic inflammation may serve as a potential modifier of parturition are discussed. Furthermore, preliminary data are presented, supporting a hypothetical model in which periodontal pathogens disseminate systemically within the mother and gain access to the foetal compartment. Several aspects of this hypothetical model remain to be elucidated. Only the clarification of the mechanisms of pathogenesis of both periodontitis and premature deliveries will ultimately allow for accurate diagnoses and successful therapies. The concept of diagnosing and treating a periodontal patient to minimise the deleterious effects of this chronic infectious and inflammatory condition on systemic conditions represents both an unprecedented challenge and opportunity to our profession (4). 

Odontogenic infection sources represent a predisposing risk factor for patients with cardiac valvular disease (CVD) awaiting cardiac valve replacement procedures or for cancer treatment (5).  The incidence and quality of odontogenic infection sources (foci) were evaluated on 152 consecutive patients (study group, SG) undergoing cardiac valve replacement and were compared to 150 age-, gender- and residence-matched non-cardiac patients (control group, CG) (5a). Overall, 218 potential and 116 facultative odontogenic foci were found in 87 (58.3%) and in 79 (51.9%) patients of the SG respectively. In comparison with the CG (48%), the incidence of potential odontogenic infection foci was significantly higher in patients scheduled for aortic valve replacement (AVR) than in those scheduled to undergo mitral valve replacement MVR (70.4% vs. 25.0%, p < 0.01). Additionally, in patients scheduled for AVR, a significantly higher number (p < 0.01) of individual potential dentogenic infection foci (1.7 vs. 0.8 foci/valve) and a higher prevalence of PD (60.2%) was seen than for patients scheduled for MVR (31.8%) or for patients without CVD (1.0 foci/valve; 39.3%; p < 0.05). Cardiologists and cardiac surgeons should play an important role in organizing oral rehabilitation of patients scheduled for valve replacement.    In another study (5b), all dental focus examinations related to patients scheduled for heart(valve) surgery and radiotherapy of the head and neck in 16 Dutch hospitals were registered during 3 months. A total number of 470 examinations were performed. Dental foci were found and treated in more than 50% of the patients examined. There was a significant difference between dentate and edentulous patients in the percentage of patients diagnosed and treated for a dental focus. More than 80% of dentate and less than 20% of edentulous patients were treated (5b). 

Odontogenic infections are a potential risk for patients who receive cervicofacial radiotherapy and should be treated before irradiation. Anaerobic microbial infections are the most common causes. A study (5c) assessed the value of the hypoxic imaging agent fluorine-18 fluoromisonidazole (FMISO) in detecting anaerobic odontogenic infections. Positron emission tomography (PET) imaging was performed at 2 h after injection of 370 MBq (10 mCi) of FMISO in 26 nasopharyngeal carcinoma patients and six controls with healthy teeth. Tomograms were interpreted visually to identify hypoxic foci in the jaw. All patients received thorough dental examinations as a pre-radiotherapy work-up. Fifty-one sites of periodontitis, 15 periodontal abscesses, 14 sites of dental caries with root canal infection, 23 sites of dental caries without root canal infection, and seven necrotic pulps were found by dental examination. Anaerobic pathogens were isolated from 12 patients. Increased uptake of FMISO was found at 45 out of 51 sites of periodontitis, all 15 sites of periodontal abscess, all 14 sites of dental caries with root canal infection, all seven sites of necrotic pulp and 15 sites of dental caries without obvious evidence of active root canal infection. No abnormal uptake was seen in the healthy teeth of patients or in the six controls. The diagnostic sensitivity, specificity, positive and negative predictive values, and accuracy of FMISO PET scan in detecting odontogenic infections were 93%, 97%, 84%, 99% and 96%, respectively. FMISO PET scan is a sensitive method for the detection of anaerobic odontogenic infections, and may play a complementary role in the evaluation of the dental condition of patients with head and neck tumours prior to radiation therapy(5c).   A dental focus usually is a localized chronic infection that under certain circumstances may result in severe local or systemic disease. The most important dental foci are periodontitis, periapical lesions, advanced carious lesions, nonvital pulp, partially impacted teeth and root tips(5d). Local effects of dental foci particularly are processes that may come to expression because of a compromised immunological defense, such as osteoradionecrosis. Systemic effects are mainly caused by transient bacteraemia which can occur spontaneously out of dental foci or after manipulations such as brushing, flossing and dental treatment. Well known examples are infectious endocarditis, fever during chemotherapy and hematogenous infections of total joint prostheses. For all patients at risk (a.o. endocarditis, endoprosthesis, chemotherapy, radiotherapy) it is important that dental foci are treated. Because in most patients the risk factors are present lifelong, a healthy dentition and a healthy periodontium are the best way of prevention(5d)

Infections of the deep neck spaces with accompanying mediastinitis are still a therapeutic problem with a high mortality(6). A study reported on three patients with deep neck space infections and accompanyingmediastinitis who had been treated in the Departments of Otorhinolaryngology at the Universities of Bochum and Essen in the past 2 years. In two patients the infection originated from a peritonsillar abscess and in one patient from an odontogenic infection.  One patient was successfully treated by a tonsillectomy and drainage of the parapharyngeal abscess in conjunction with a thoracotomy because of a mediastinal abscess and bilateral pneumothorax. The second patient was cured by a tonsillectomy, wide cervical drainage und cervical mediastinotomy(6). 

A study reported two cases of septic pulmonary embolism associated with periodontitis (8). Both patients had toothache, fever, and chest pain, and showed findings of periodontitis at initial presentation. Antimicrobial agents combined with dental surgery were successful in treatment. While septic pulmonary embolism from the lesions of periodontitis appears to be rare, periodontitis remains important in the differential diagnosis of septic pulmonary embolism.

One study found a positive correlation between higher levels of periodontal disease and various types of rheumatic conditions, as well as with various alterations of saliva flow, including slower flow rates and higher levels of  immune reactivity(9). This was consistent with autoimmunity commonly found in some of these rheumatic conditions. 

 

Odontogenic sinusitis is a well-recognized condition and accounts for approximately 10% to 12% of cases of maxillary sinusitis(10). An odontogenic source should be considered in individuals with symptoms of maxillary sinusitis with a history of odontogenic infection, dentoalveolar surgery, periodontal surgery, or in those resistant to conventional sinusitis therapy. Diagnosis usually requires a thorough dental and clinical evaluation including appropriate radiographs. The most common causes of odontogenic sinusitis include dental abscesses and periodontal disease that had perforated the Schneidarian membrane, irritation and secondary infection caused by intra-antral foreign bodies, and sinus perforations during tooth extraction. An odontogenic infection is a polymicrobial aerobic-anaerobic infection, with anaerobes outnumbering the aerobes. The most common isolates include anaerobic streptococci and gram-negative bacilli, and Enterobacteriaceae. Surgical and dental treatment of the odontogenic pathological conditions combined with medical therapy is indicated. When present, an odontogenicforeign body should be surgical removed(10a).  Although odontogenic sinusitis is a rare entity when compared to sinus disease of rhinogenic origin, it is extremely important to identify a dental aetiology when it occurs. The offending tooth or teeth would thus require endodontic treatment or extraction, and the sinus disease carefully assessed and appropriately managed(10c). Certain lesions such as cysts and tumours may involve the jaws and hence the maxillary antrum; some of these, such as a radicular cyst are quite common.  

Another study presented a case of periapical infection resulting in unilateral maxillary sinusitis and cellulitis of the ipsilateral lower eyelid(10d), while another provided a case of a pathogenic fungus infecting the sinus related to a dental infectious source(10e). This pathogenic fungus is very invasive, particularly in immunodepressed or immunocompromised patients.

Movement disorders - or dyskinesias - are characterized by involuntary movements.  A review found a significant association between dental conditions and some common dyskinesias, viz., Gilles de la Tourette's syndrome, Huntington's disease, idiopathic torsion dystonia, oral dyskinesias, and Parkinson's disease(11). Generalized dyskinesias were found to have focal manifestations in the orofacial region. 

The association of alopecia areata and infectious foci of dental origin is relatively common, and may be explained by the autoimmune nature of the disorder (12,29). A study described a case of alopecia areata with no apparent cause and that was effectively resolved by eliminating a focalized dental infection via endodontic treatment. The presence of common immune mediators in the pathogenesis of both alopecia areata and dental infection could account for the dental origin of the hair loss. In this sense, patients with localized alopecia should be subjected to careful exploration of the oral cavity in search of possible dental infections.

Health Effects Related to Root Canals

Studies have found that all root canaled teeth with asymptomatic apical periodontitis contain anaerobic bacteria and are a significant source of bacteria and fungi in the circulating blood, and thus a potential source of systemic focal infections (13,26-31).  One study (13a) used phenotypic and genetic methods to trace microorganisms released into the bloodstream during and after endodontic treatment back to their presumed source--the root canal. Microbiological samples were taken from the root canals of 26 patients with asymptomatic apical periodontitis of single-rooted teeth. The blood of the patients was drawn during and 10 minutes after endodontic therapy. All root canals contained anaerobic bacteria. The frequency of bacteremia varied from 31% to 54%. The microorganisms from the root canal and blood presented identical phenotype and genetic characteristics within the patients examined. The study demonstrated that endodontic treatment can be the cause of anaerobic bacteremia and fungemia.  In another study (13b) quantitation of circulating immune complexes (CIC) was done in 45 patients with chronic periapical lesions. The levels were compared with those of age-matched healthy individuals. Both patients with chronic periapical granuloma and periapical cysts showed significantly higher levels of CIC than the controls. This observation indicates that the continuous presence of root canal antigens may cause elevated levels of circulating immune complexes. The possibility of chronic periapical lesions acting as foci of infection is discussed, and the importance of early treatment of these conditions is emphasized. The so-called focal infections are today considered to be polyetiologic manifestations, in which there is a summation of various aggressions(13c). Bacterial products, toxic or antigenic substances originating from different foci are but one of the elements susceptible of causing disease. Scientific evidence shows that the histologic result of an apicectomy is considerably worse than the radiological evidence might lead to believe(13c,29). Inflammation may persist for years before it disappears. Radiographs are therefore only a coarse criterion for judging results of healing. When facing a disease caused by focal infection, the possible foci should be eliminated quickly and as radically as possible(13c,10).  Another study found root-canaled teeth to be a risk factor in hospital treatment of conditions such as heart valve replacement and cancer treatment(4c,29-32).  

Endodontic infections have been traditionally studied by culture methods, but recent reports showing that over 50% of the oral microbiota is still uncultivable(13d) (B. J. Paster et al., J. Bacteriol. 183:3770-3783, 2001) raise the possibility that many endodontic pathogens remain unknown. This study investigated the prevalence of several uncultivated oral phylotypes, as well as newly named species in primary or persistent endodontic infections associated with chronic periradicular diseases. Samples were taken from the root canals of 21 untreated teeth and 22 root-filled teeth, all of them with radiographic evidence of periradicular bone destruction. Genomic DNA was isolated directly from each sample, and 16S rRNA gene-based nested or heminested PCR assays were used to determine the presence of 13 species or phylotypes of bacteria. Species-specific primers had already been validated in the literature or were developed by aligning closely related 16S rRNA gene sequences. Species specificity for each primer pair was confirmed by running PCRs against a panel of several oral bacteria and by sequencing DNA from representative positive samples. All species or phylotypes were detected in at least one case of primary infections. The most prevalent species or phylotypes found in primary infections were Dialister invisus(81%), Synergistes oral clone BA121 (33%), and Olsenella uli (33%). Of the target bacteria, only these three species were detected in persistent infections. Detection of uncultivated phylotypes and newly named species in infected root canals suggests that there are previously unrecognized bacteria that may play a role in the pathogenesis(13d).  Patients suffering from auto-immune disease affecting the heart often become quite well when the offending root canal infected tooth is removed (4f,29,31).

A study (13e) developed to assess the differences in sealed versus unsealed root-canals followed the development of periapical lesions both radiographically and histologically in infected teeth with open and sealed root canals. The mandibular premolars from five adult monkeys were used in the experiment. Sealed infected teeth developed radiographic signs of periapical pathosis significantly earlier than unsealed teeth. Although, histological signs of pathology could be seen periapically at earlier observation periods, sealed teeth consistently developed these changes earlier than unsealed teeth. Furthermore, the histological periapical pathology differed somewhat between the two groups in that unsealed teeth showed a multi-focal diffuse pattern of spreading. 

Studies have demonstrated an association between infective endocarditis and dental procedures including root canals and gum scaling (14). A study was undertaken to assess the relative risk of infective endocarditis associated with various dental problems and procedures and the protective efficacy of antibiotic prophylaxis by a case-control study(14a). Cases (n = 171) and controls were matched as regards sex, age and underlying cardiac condition. They were requested to indicate all the medical, surgical or dental procedures within the previous 3 months. Dental scaling and root canal treatment showed a trend towards a higher risk of infective endocarditis (P = 0.065). The 46% protective efficacy of antibiotic prophylaxis was not significant. Our data suggest that surgery should be more clearly mentioned in future guidelines regarding dental conditions, and reemphasize that a rigorous treatment of any focal infection in cardiac patients is mandatory. From the efficacy rate of antibiotic prophylaxis, it can be estimated that the overall incidence of infective endocarditis might be reduced by 5 to 10% in France by appropriate use of antibiotic prophylaxis in cardiac patients.

Many researchers and cancer treatment clinics have observed or documented a connection between cancer and root-canals.  Many cancer treatment clinics require elimination of root-canals before treatment due to their experience with the cancer/root-canal connection (22,25,32) 

One study (15) described a remission of rheumatoid arthritis (RA) of 16 years duration, apparently caused by the extraction of endodontically well-treated, healthy looking root-canaled teeth.  After extraction, a small pus layer was found to cover the apices of the clinically healthy looking teeth. The rheumatoid factor (RF) became negative and the patient remained symptom free for the next 16 years.  

In another study (16) a severe periodontal condition occurred in 58% of 77 rheumatic patients of various rheumatoid conditions compared with only 26% of the controls (p < 0.0001). The severity of focal sialadenitis correlated significantly with salivary IgA, IgG, and IgM concentrations. Salivary albumin, total protein, IgG, and IgM concentrations were higher in all patient groups than in the controls. The number of patients with low salivary flow rates was higher in all patient groups compared to controls. Patients with rheumatic diseases, irrespective of specific diagnosis, thus had various alterations in salivary flow and composition and oral health. The findings may reflect the autoimmune inflammation of the salivary glands frequently observed in these patients

 

A possible and diagnostically difficult source of bacterial sepsis appears to be pus related foci of odontogenic character.  One study (17) describes a case of a pregnant woman, in whom an untreated purulent focus within the oral cavity led to severe systemic infection characterized by persistent hectic fever with accompanying features of intravascular coagulation, anemia and erythema nodosum and no response to antibiotic treatment. It was the second episode of sepsis in this patient in a period of one year, the source of the infectious process not being recognized previously. Dental examination revealed presence of the apical abscess of the tooth 6-, extraction of which led to spectacular clinical improvement, accompanied by the healing of erythema nodosum. Purulent foci within oral cavity, including apical abscesses, constitute significant clinical problems and must be taken into consideration as a potential source of severe and recurrent systemic infections.

A 71-year-old male with coronary artery disease, hypertension, diabetes mellitus, and tobacco dependence came to the emergency room complaining of one episode of retrosternal chest pain oppressive in nature of one day of evolution (18). He had acute respiratory distress and required mechanical ventilation. During the following hours, neck and tongue edema developed. Dental examination revealed a submandibular abscess which was drained. The source of infection was found on the second molar of the left lower jaw. After extraction and antibiotic treatment, the patient improved and was successfully weaned from mechanical ventilation. 

Cavitations

Ischemic jawbone lesions were first discussed in the dental literature more than a century ago, but then seemingly forgotten. In recent years, there has been considerable resurgence in interest and studies in this unique pathological condition (10,19,29-31). Controversy surrounds the subject. A study (19a) attempted to assess if there are common diagnoses of jawbone pathologies that produce pain?  A review was made of the clinicopathologic features of 500 consecutive jawbone surgeries with pathological confirmation in patients with idiopathic facial pain. Four hundred seventy-six (476) of the 500 lesions (95.2%) were directly attributed to impaired blood flow in the jawbone, tooth, or both, according to histopathological analysis and confirming Cavitat (bone ultrasound) examination. Statistical data concerning the location, frequency, and pathological diagnoses of these bony lesions was presented, as are brief methods of diagnosis, and treatment was also discussed(19a).

In a group of 38 patients with chronic oral pain in the area where teeth had been extracted, approximately 90% of subpontic bone demonstrated either ischemic osteonecrosis (68%), chronic osteomyelitis (21%), or a combination (11%) (19b) . More than 84% of the patients had abnormal radiographic changes in subpontic bone, and 5 of 9 (56%) patients who underwent radioisotope bone scan revealed hot spots in the region. Of the 14 patients who had laboratory testing for coagulation disorders, 71% were positive for thrombophilia, hypofibrinolysis, or both (normal: 2% to 7%). Ten pain-free patients with abnormal subpontic bone on radiographs were also reviewed.  Intraosseous ischemia and chronic inflammation were suggested as a pathoetiologic mechanism for at least some patients with atypical facial pain. These conditions were also offered as an explanation for poor healing of extraction sockets and positive radioisotope scans(19b). Many cases are discussed in (29-31,10).

All bones of the facial skeleton and spine are susceptible to osteomyelitis due to various predisposing conditions(19c). Current radiological tools are sufficient to provide adequate diagnosis. Treatment can be conservative resection of the diseased bone with adequate clearance in all cases except in cases of osteomyelitisdue to osteoradionecrosis (ORN) where resection has to be more radical. Dealing with osteomyelitis in head and neck bones is not the same as in other bones of the body due to the nature of the bones, complex anatomy of the region, and esthetics. The study analyzed the behavior of osteomyelitis in the head and neck bones and its management.  A total of 84 cases of osteomyelitis in head and neck were reviewed in a 10-year period. Pus for culture, antibiotic sensitivity, and radiology were the main investigations. A medical line of treatment was effective in acute cases. Surgery was opted for in chronic cases.  Mandible, frontal bone, cervical spine, maxilla, temporal bones, and nasal bones were involved, in descending order of frequency, i.e. the mandible was the most common bone affected. Nine patients were diagnosed as having acute osteomyelitis (11%); 75 were diagnosed as having chronic osteomyelitis (89%). Radiation-induced ORN leading to osteomyelitis was the most common cause ofosteomyelitis of the mandible (13 of the 32 cases; 41%). Odontogenic infections and chronic sinusitis each gave rise to osteomyelitis in 3 of 10 cases (30%) of the patients with osteomyelitis of the maxilla. Chronic sinusitis was associated with frontal bone osteomyelitis in all 20 cases (100%). Tuberculosis (10 of 15 cases; 67%) and malignancy (5 of 15 cases; 33%) were the main predisposing factors in cervical spine osteomyelitis. Malignant external otitis (MEO) with diabetes mellitus was associated with all four cases of osteomyelitis of the temporal bone. Of the 18 patients with a diagnosis of ORN, the mandible was found to be the most susceptible bone (13 cases; 72%), followed by the maxilla (four cases; 22%) and cervical spine (1 case). Acute osteomyelitis responded in some degree to antibiotics. Sequestrectomy was carried out in all chronic cases but in cases of ORN more radical surgery was performed(19c).

Cerebral abscess is a rare but serious and life-threatening infection. Dental infections have occasionally been reported as the source of bacteria for such an abscess (20,29-31). A 54-year-old man was admitted with a right hemiparesis and epileptic fits. After clinical, laboratory and imaging examination, the diagnosis of a cerebral abscess of the left parietal lobe was made. The intraoral clinical examination as well as a panoramic radiograph confirmed the presence of generalized periodontal disease, multiple dental caries, and periapical pathology.  After removal of the periodontal, decayed and periapically involved teeth of the patient and treatment of the abcess the patient recovered. 

 

A patient had 2 episodes of pneumococcal meningitis with bacteraemia and 2 episodes of bacteraemia without meningitis during a 1-y period (21). Investigations using bone and leukocyte scintigraphy revealed a focal uptake in the right mandibular bone (cavitation).

A study presented an unusual case of chronic osteomyelitis with proliferative periostitis affecting the mandible of a 12-year-old patient (23). The source of infection was related to the developing lower left third molar, which had apparently no communication with the oral cavity. Chronic osteomyelitis with subperiosteal new bone formation results from periosteal reaction to chronic inflammatory/infectious stimulation. In the maxillofacial region, it has traditionally been termed Garrè's osteomyelitis with proliferative periostitis and more recently periostitis ossificans. 

Research and clinical experience of several doctors have confirmed that root canal teeth, cavitations, and other oral infections commonly cause chronic neurological and immune conditions as well as cancer (26-32,10).     

References

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3. (a) Periodontal infections and cardiovascular disease: the heart of the matter. J Am Dent Assoc. 2006 Oct;137 Suppl:14S-20S; quiz 38S, Demmer RT, Desvarieux M; & (b) An update on infective endocarditis of dental origin. J Dent.2002 Jan;30(1):37-40. Tomás Carmona I, Diz Dios P, Limeres Posse J, et al; & (c) The role of chronic dental bacterial infections in the aetiopathogenesis of ischaemic heart disease] [Article in Polish] Wiad Lek. 2002;55 Suppl 1(Pt 2):922-6. Stypułkowska J, Lyszczarz R, Błazowska K; & (d) Cardiovascular and oral disease interactions: what is the evidence? Prim Dent Care. 2007, Apr; 14(2):59-66. Ford PJ, Yamazaki K, Seymour GJ; & (e) Cardiovascular disease and periodontal diseases: commonality and causation. Compend Contin Educ Dent. 2004 Jul;25(7 Suppl 1):26-37. Dave S, Batista EL Jr, Van Dyke TE; & (f) Oral health, atherosclerosis, and cardiovascular disease.  Crit Rev Oral Biol Med. 2004 Nov 1;15(6):403-

10. The International Academy of Oral Medicine and Toxicology, IAOMT, Jawbone Osteonecrosis; & Root Canal Dangers, Dr, Hal Huggins, https://iaomt.org/root-canal-dangers/; & The International Academy of Oral Medicine and Toxicology, IAOMT, IAOMT Commentary on the Risks of Root Canal 

13. Meurman JH, Sanz M, Janket SJ; & (g) Life-threatening thrombotic thrombocytopenic purpura associated with dental foci. Report of two cases.  J Clin Periodontol. 2004 Nov;31(11):1019-23, Fenner M, Frankenberger R, PressmarK, John S, Neukam FW, Nkenke E; & (h) Update on general health risk of periodontal disease.  Int Dent J. 2003;53 Suppl3:200-7. Slots J; &  (i) The Connection between Dental Related Gum Disease and Heart Diseasesee (29.);  & (j) Is periodontal disease a risk factor for coronary artery disease (CAD)? J Can Dent Assoc. 2002 Mar;68(3):176-80.  Lavelle C; & (k) Strength of evidence linking oral conditions and systemic disease. Compend Contin Educ Dent Suppl. 2000;(30):12-23, Joshipura K, Ritchie C, Douglass C 

4.  Periodontal medicine: emerging concepts in pregnancy outcomes. J Int Acad Periodontol. 2000 Jan;2(1):9-13, Champagne CM, Madianos PN, Lieff S et al; 

5. (a) Odontogenic infection sources in patients scheduled for cardiac valve replacement. Oral Health Prev Dent.2007;5(2):153-9.  Krennmair G, Auer J, Krainhöfner M, Piehslinger E; & (b)[Diagnosing and treatment of dental foci in Dutch medical centres] [Article in Dutch]  Ned Tijdschr Tandheelkd. 2007 Jul;114(7):287-91, Gortzak RA, van der Waal I, Allard RH; & (c) Detection of anaerobic odontogenic infections by fluorine-18 fluoromisonidazole.  Eur J Nucl Med. 1996 Oct;23(10):1384-7, Liu RS, Chu LS, Yeh SH et al; & (d) Dental foci. Role, treatment and prophylaxis in patients at risk] Ned Tijdschr Tandheelkd. 1998 Feb;105(2):52-6 [Article in Dutch] Jansma J, Vissink A.

6. Infections of the deep neck spaces with accompanying mediastinitis] [Article in German] Laryngorhinootologie. 2005 Mar;84(3):171-5; Lautermann J, Lehnerdt G, Beiderlinden M, Sudhoff H.

8. Septic pulmonary embolism associated with periodontal disease: reports of two cases and review of the literature. Chest. 2002, Feb; 121(2):652-4. Shiota Y, Arikita H, Horita N, Hiyama J, Ono T, Ohkawa S, Yamakido M.

9. Oral and salivary parameters in patients with rheumatic diseases.  Acta Odontol Scand. 2005 Oct;63(5):284-93, Helenius LM, Meurman JH, Lindqvist C. et al. 

10. (a) Sinusitis of odontogenic origin.  Otolaryngol Head Neck Surg. 2006, Sep; 135(3):349-55, Brook I; & (b)  Chronicodontogenic maxillary sinusitis. Stomatologija. 2006;8(2):44-8. Ugincius P, Kubilius R, Gervickas A, Vaitkus S; & (c)  Clinical update--the teeth and the maxillary sinus: the mutual impact of clinical procedures, disease conditions and their treatment implications. Part 2. Odontogenic sinus disease and elective clinical procedures involving the maxillary antrum: diagnosis and management. Aust Endod J. 1999 Apr;25(1):32-6, Sandler HJ; & (d) Orbital cellulitis as a sole symptom of odontogenic infection. Singapore Med J. 1999 Feb;40(2):101-3. Ngeow WC; & (e) [Uncommon fungal maxillary sinusitis of dental origin due to Scedosporium prolificans]  Rev Stomatol Chir Maxillofac. 1995;96(2):66-9, [Article in French] ChikhaniL, Dupont B, Guilbert F, Bertrand JC, Improvisi L, Corre A  

11. Dental implications of some common movement disorders: a concise review.  Arch Oral Biol. 2007 Apr;52(4):395-8. Epub 2006 Nov 27, Lobbezoo F, Naeije M.

12. Alopecia areata of dental origin. [Article in English, Spanish] Med Oral. 2002 Jul-Oct;7(4):303-8, Gil Montoya JA, Cutando Soriano A, Jimenez Prat J.

13. Anaerobic bacteremia and fungemia in patients undergoing endodontic therapy: an overview. Ann Periodontol. 1998 Jul;3(1):281-7, Debelian GJ, Olsen I, Tronstad L; & (b) Quantitation of circulating immune complexes in patients with chronic periapical lesions.  J Nihon Univ Sch Dent. 1993 Sep;35(3):175-8. Anil S, Shanavas KR, Beena VT, Remani P, Vijayakumar T; & (c ) Apicoectomy and focal diseases] [Article in French], Held AJ.  SSO Schweiz Monatsschr Zahnheilkd.1975 Feb; 85(2):190-204; &  (d)    Uncultivated Phylotypes and Newly Named Species Associated with Primary and Persistent Endodontic Infections, J Clin Microbiol. 2005 July; 43(7): 3314–3319.   J. F. Siqueira, Jr.* and I. N. Rôças; & (e) Development of periapical lesions. Swed Dent J. 1993; 17(3):85-93, Jansson L, Ehnevid H, Lindskog S, Blomlöf L.; & (f)Dr. James Howenstine -- What You Need to Know About Root Canals www.newswithviews.com/Howenstine/james34.htm

14. (a) Procedures associated with infective endocarditis in adults. A case control study.  Eur Heart J. 1995 Dec;16(12):1968-74, Lacassin F, Hoen B et al; &  (b) Root canal treatment and general health: a review of the literature.  Int Endod J. 2000 Jan;33(1):1-18.  Murray CA, Saunders WP; & (c) 14. (c) Serious complications of endodontic infections: some cautionary tales. Aust Dent J. 1997 Jun;42(3):156-9, Walsh LJ; & (d) Detection of bacterial virulence genes associated with infective endocarditis in infected root canals. Int Endod J. 2000 May;33(3):194-203, Bate AL, Ma JK, Pitt Ford TR.   

15. 16-year remission of rheumatoid arthritis after unusually vigorous treatment of closed dental foci. Clin Exp Rheumatol.2002 Jul-Aug;20(4):555-7, Breebaart AC, Bijlsma JW, van Eden W.

16. Oral and salivary parameters in patients with rheumatic diseases.  Acta Odontol Scand. 2005 Oct;63(5):284-93, Helenius LM, Meurman JH, Lindqvist C. et al. 

17. [Severe form of odontogenic sepsis--a case report] Pol Merkur Lekarski. 2005 Mar;18(105):314-6. Pryszmont J, Grygorczuk S, Kondrusik M, et al. 

18. Ludwig's angina: an uncommon cause of chest pain. South Med J. 2005 May; 98(5):561-3.  Ocasio-Tascón ME, Martínez M, Cedeño A, et al.

19. (a) Medullary and odontogenic disease in the painful jaw: clinicopathologic review of 500 consecutive lesions.  Cranio.2002 Oct;20(4):295-303, Shankland WE; & (b)  Ischemic osteonecrosis under fixed partial denture pontics: radiographic and microscopic features in 38 patients with chronic pain. J Prosthet Dent. 1999 Feb;81(2):148-58, Bouquot JE, LaMarcheMG; & (c) Osteomyelitis in the head and neck.  Acta Otolaryngol. 2007 Feb;127(2):194-205. Prasad KC, Prasad SC, MouliN, Agarwal S; & (d) Case # 9. Focal sclerosing osteomyelitis.  J Indiana Dent Assoc. 2002 Spring;81(1):27-8, Adams WR.

20. Cerebral abscess of odontogenic origin. J Craniomaxillofac Surg. 2007 Jan;35(1):63-7. Epub 2007 Feb 12.  Mylonas AI, Tzerbos FH, Mihalaki M, Rologis D, Boutsikakis I.

21. Recurrent Pneumococcal bacteraemia and meningitis in an asplenic adult with possible unusual focus. Scand J Infect Dis.2001;33(9):706-8,Kragsbjerg P,Rydman H 

22. (a)  Root Canals & Cancer (isselsdiamond,huggins)

http://www.whale.to/d/root2.html

 

 

22. (b)  Many cancer doctors in Europe and elsewhere urge removal of root canal teeth before cancer fighting treatments are administered. http://www.annieappleseedproject.org/dentalissues.html

 

22. (c ) The Relationship Between Root Canals and Cancer, Independent Cancer Research Foundation,  http://www.new-cancer-treatments.org/Articles/RootCanals.html

22. (d) Dr. Robert Kulacz's The Roots of Disease: Connecting Dentistry and Medicine, Root Canals and Cancer,    see (29-31) 

22. (e) Cancer Care Expert Details Root Canal Case Studies

https://www.westonaprice.org/health-topics/dentistry/root-canal-dangers/

 

 22. (f) Root Canal Cover Up + Milk Proteins (1996) (Vol 11 (1)) The Gerson Institute

http://www.gerson.org/store/ProductDetail.asp?id=N9959

 

22. (g) Chronic Illness, Cancer, Root Canals, and Cavitations-  see(29-31)

 

22.(h) Central (intraosseous) adenoid cystic carcinoma of the mandible: report of a case with periapical involvement. J Endod. 2000 Dec;26(12):760-3, Favia G, Maiorano E, Orsini G, Piattelli A.

23.  Osteomyelitis with proliferative periostitis: an unusual case.  Or al Surg Oral Med Oral Pathol Oral Radiol Endod. 2006 Nov;102(5) Tong AC, Ng IO, Yeung KM.

25. ROOT CANALS POSE HEALTH THREAT - AN INTERVIEW WITH GEORGE MEINIG, D.D.S    http://www.rheumatic.org/teeth.htm   & www.kinesiology.nu/hdentistry/root.html

26. Six Common Dental Procedures That can Harm Your Health, and How Environmental Dentistry (aka Holistic or Biological Dentistry) can Help,  By Lina C. Garcia, D.D.S., D.M.D.  www.mercola.com/2004/feb/18/dental_health.htm

 

28. Death and Dentistry, Martin Fischer — 1940 Charles Thomas and Co., Springfield, Ill,  www.road-to-health.com/books/42/42.pdf

 

29. Toxic Root Canals, Dr. T. Levy, The Toxic Tooth;& Dr. J. Mercola, Root Canals Linked to Heart Disease and Inflammatory Conditions,; & TOXIC BACTERIA IN TEETH CONTRIBUTES TO ILLNESS THROUGHOUT THE BODY,

30.  Root Canal Coverup, Dr. G.Meinig DDS; & https://www.foodmatters.com/article/root-canal-cover-up-exposed: & Weston Price findings,

31. The Roots of Disease, Dr. T Levy, & Hidden Epidemic, Silent Oral Infections cause most heart attacks and Breast Cancer, Dr. T Levy,2017

32. Cancer/Root Canals   https://www.cancertutor.com/advdental/