The theory of focal infection postulates that a myriad of diseases are caused by microorganisms (bacteria, fungi and viruses) that arise endogenously from a focus of infection. In 1890, the dentist WD Miller published his treatise: The Microorganisms of the Human Mouth: The Local and General Diseases Which Are Caused by Them [1]. In 1900, the English physician William Hunter reported that the preservation of the dentition by dental treatment was a cause of a multitude of diseases attributed to focal infection [2]. In 1911 his remarks to medical students at McGill University in Montreal ignited the fires of focal infection further with unfounded reports of gold fillings, crowns and bridges and fixed dentures, built on and about diseased tooth roots forming a mausoleum over a mass of sepsis to which there is no parallel in the whole realm of medicine and surgery [3]. In 1912 Frank Billings formally and independently introduced the concept of focal infection to American physicians, highlighting case reports ascribing distant infections to various pathogens and claiming cures for these afflictions by tonsillectomies and dental extractions as a means to removal of these various foci of infections [4]. EC Rosenow, a pupil of Billings, further developed the theories of ‘elective localisation’ and ‘transmutation’, whereby microorganisms could possess affinities for certain body organs and then alter their biological characteristics [5].

In the 1920s, Dr Weston Price published a series of rabbit experiments and case reports of extraordinary improvements in various medical conditions after dental extractions [6]. Endodontics came under particular scrutiny with advocates of Hunter, Billings, Rosenow and West recommending that all infected non-vital teeth should be removed rather than endodontically treated to prevent or cure focal infections. Further researchers presented the idea of microorganism’s dissemination, or their associated toxins throughout the body formed a focus of circumscribed infection at a particular site, which could exacerbate systemic disease or damage to a distant tissue. These ideas were based on limited scientific research, few controlled studies and anecdotal evidence, yet produced a reaction that was so strong that the teaching of clinical endodontic techniques was stopped altogether in most American institutions in favour of dental extractions [7]. Despite lack of robust evidence to the contrary, there is still an international body of dental practitioners who refuse to perform root canal treatment, reciting the research performed 80–90 years ago to justify their cause.

Numerous studies have attempted to determine the risk of bacteraemia associated with lesion of endodontic origin following nonsurgical and surgical endodontics. A bacteraemia is far more probable if root canal instrumentation is carried out beyond the apex of the tooth rather than maintained within the confines of the canal [8]. A further study in 1976 investigating bacteraemia subsequent to surgical and nonsurgical root canal treatment corroborated the findings of no bacteraemia being produced if root canal treatment was limited to within the canal. The authors demonstrated that nonsurgical root canal treatment resulted in a much lower bacteraemia incidence (3.3 % due to overinstrumentation), compared to flap reflection (83.3 %), peri-radicular curettage (33.3 %) or tooth extraction (100 %) [9, 10]. In the 1990s, with the advent of modern aseptic sampling techniques, methods of identification using DNA probes and effective transport mediums, further evidence has been provided into the nature of bacteria that may be found whether instrumentation was carried out within the canal itself or overinstrumented. Taken together these studies demonstrated that greater numbers of bacteraemia result from root canal procedures, anaerobic species were commonly associated and even when instrumentation was confined to the canal itself a bacteraemia was possible [11–13].

The use of rubber dam clamps, wedges and matrix bands has also been demonstrated as causing cumulative bacteraemia relative to tooth extractions [14, 15]. It is reasonable to conclude that nonsurgical endodontics may be the least likely of dental procedures to produce a significant bacteraemia, but antibiotic prophylaxis may be indicated for the prevention of endocarditis in susceptible patients according to which country you reside in. Nevertheless, to date, no interventional studies have been performed to support the evidence that modern endodontic therapy is not safe and effective [14, 15].

Damage or injury to the cardiac valves (most commonly mitral and aortic) can result in a layer of platelets and fibrin deposits (nonbacterial thrombotic endocarditis or vegetation), which can incorporate circulating bacteria and fungi resulting in bacterial or infective endocarditis (IE). The undoubted role of oral bacteria and in particular the viridans group streptococci (VGS) and staphylococci has led to the hypothesis that oral bacteria enter the circulation during invasive dental procedures [16].

Numerous expert committees in different countries have proposed different antibiotic prophylactic (AP) regimens for the prevention of IE. These include the British Society for Antimicrobial Chemotherapy (BSAC) (UK) [17], European Society of Cardiology (Europe) [18], American Heart Association (USA) [19] and the Infective Endocarditis Prophylactics Expert Group (Australia) [20]. The AP guidelines for the prevention of IE have undergone various periodic revisions with a progressive restriction for the indications of AP. In the UK, the National Institute for Health and Clinical Excellence (NICE) published new guidelines in 2008 [21], which proposed that ‘AP against IE is not recommended for people undergoing dental procedures’. This proposal was applied even to the highest-risk patients, independently of the type of dental procedure they were undergoing.

The main argument against the administration of AP for the prevention of distant site infections and, specifically, of IE secondary to dental procedures in patient considered to be at risk is the efficacy of such regimes [22]. Daily activities such as mastication and toothbrushing and flossing result in a similar bacteraemia that occurs following invasive dental procedures such as extractions [23]. Other arguments against the use of AP for IE include the development of β-lactam antibiotic resistance, risk of anaphylaxis and allergy and costs to health care systems [24].

As a result, some cardiologists remain understandably concerned about the omission of AP. In general the main guidelines in Europe, the USA and Australia continue to recommend the administration of AP, though restricting its indications (see Tables 18.1, 18.2 and 18.3). It would therefore appear reasonable to adopt the recommendations proposed by the expert committees in the country of your practice liaising with the patients’ cardiologist to confer prophylaxis indicated.

Joint replacement is a proven cost-effective medical procedure that started from hip replacements in the 1950s expanding to include knee, ankle, shoulder, and elbow and finger joints. Infection following a joint replacement is a devastating complication that can be divided into early and late occurring. Early infections that is within the first 3 months following implantation primarily relate to infection introduced at the time of the operation, either sourced from the patient or the surgical staff. Late infections, more than 3 months after primary implantation, are usually secondary to bacteraemia [25].

There are a number of antibiotic prophylaxis guidelines which have been produced by national bodies. In July 2003, the American Dental Association published an advisory statement in association with the American Academy of Orthopaedic Surgeons: ‘Antibiotic prophylaxis is not routinely indicated for most dental patients with total joint prosthesis but it may be advisable to consider pre-medication in a small number of patients who may be at potential risk of experiencing haematogenous joint infections’. This is a major change in attitude by the Americans [26]. The British National Formulary has a similar analysis, which looks at the rationale behind the guidelines and examines the issues from a risk management point of view. It emphasises that the risk of antibiotic prophylaxis outweighs the risk of joint infection. It also emphasises the need for communication between orthopaedic surgeons and dentists. It confirms that within broad guidelines all patient situations are individual and this requires individual communication, co-operation and treatment plans [27].

The Australian guidelines agreed that antibiotic prophylaxis was only indicated for high-risk dental procedures in immunocompromised patients with joint problems (see Table 18.4). Prior to joint replacement, all patients should be deemed dentally fit, and an appropriate oral review should be made to determine this. Dental treatment during the preimplantation phase should be aggressive to eliminate any foci of infection. During the first 3 months following joint replacement, if a dental infection arises, it should be treated aggressively by endodontics or extraction with appropriate therapeutic antibiotics. Following this interim 3-month period once the joint prosthesis is functioning well and is stabilised, routine dental treatment including extractions should be carried out without any antibiotic prophylaxis. Patients who are deemed high risk of developing an infection (i.e. have already had a previous episode of joint replacement for an infected prosthesis or immunocompromised) may require standard antibiotic prophylaxis. Effective communication with the patients’ orthopaedic surgeon is essential, and in situations where prophylaxis is requested, it needs to be recorded so that the responsibility for any adverse outcome related to the administration of antibiotic therapy lies with the requesting clinician [25].

The detrimental effects of radiotherapy, chemotherapy and ablative surgery to the dentition and oral health necessitate extraction of at-risk teeth. This includes all carious and heavily restored teeth, teeth with deep periodontal pockets and inaccessible posterior teeth. The side effects of radiotherapy depend on the dose, delivery (number of fractions), site and mode and can result in xerostomia, mucositis, trismus, radiation caries and osteoradionecrosis (ORN) developing later.

ORN is a condition of exposed, devitalised bone for greater than 3 months in an area that has been irradiated. This arises due to radiation-induced free-radical species, endothelial changes, inflammation, fibrosis and necrosis. The exposed bone can then be superinfected by oral microorganisms [28]. Endodontic treatment in the irradiated patient may result in challenges complicated by the presence of trismus and limited inter-occlusal space preventing ideal access cavity preparation. Nevertheless it may be preferable to extraction, thereby minimising the risk of ORN [29].

Diabetes mellitus is a group of diseases characterised by high levels of blood glucose resulting from defects in insulin production, insulin action or both. Type I diabetes, or insulin-dependent diabetes mellitus, is an autoimmune disease that causes the destruction of insulin-producing β-cells in the pancreas. Type 2 diabetes, or non-insulin-dependent diabetes mellitus is characterised by resistance of insulin and inadequate insulin production [30].

As a consequence, this disease promotes hyperglycaemia, wound healing difficulties as well as systemic and oral manifestations. Experimental and clinical studies have demonstrated a higher prevalence of peri-apical lesions in patients with uncontrolled diabetes. Pulps from patients with diabetes have the tendency to present limited dental collateral circulation, impaired immune response and increased risk of acquiring infection (especially anaerobic ones) or necrosis. With regard to molecular pathology, hyperglycaemia is a stimulus for bone resorption, inhibiting osteoblastic differentiation and reducing bone recovery. Patients with diabetes have increased periodontal disease in teeth involved endodontically and have a reduced success of endodontic treatment in cases with preoperative peri-radicular lesions [31, 32].

Osteoporosis is defined as a skeletal disorder that compromises bone strength, predisposing a person to an increased risk of bone fracture due to inhibited calcium intake and mineral loss. Osteoporosis can be classified as primary occurring in both genders at all ages, typically following menopause in women and occurring later in life in men. Secondary osteoporosis is the result of medications (glucocorticosteroids) or as a result of diseases such coeliac disease or cystic fibrosis.

Bisphosphonates are the primary drugs used to treat osteoporosis by suppressing osteoclast activity and increasing bone mineral density. Patients treated with intravenous bisphosphonates have a risk of developing bisphosphonate-related osteonecrosis (BRONJ) of the jaw. This risk increases when the duration of therapy exceeds 3 years. As this condition is debilitating and difficult to treat, all efforts should be made to prevent its occurrence. The main triggering event is considered to be dental extraction. Nonsurgical endodontic treatment is a safe alternative to dental extractions, but caution should be mandatory with particular attention to treatment protocols to avoid the risk of developing BRONJ (see Table 18.5) [33].