Prospective, longitudinal assessment of quality of life inpatients with cancer of the head and neck and their primary carers

Cancer of the head and neck has profound psychosocial and physical effects on patients, so quality of life (QoL) is an essential consideration—not only is it of importance to the patient but it also provides a subjective measure of the success of treatment. However, we know of little work about its influence on carers. The aim of this study was to assess the impact of the diagnosis and treatment on the QoLof patients and their carers from baseline (preoperatively) to three months postoperatively. Thirty-six patients and 21 primary carers were enrolled, and patients completed one head-and-neck-specific measure, the University of Washington Head and Neck, Version Four (UW-V4),and three other questionnaires, both at the time of diagnosis and at one and three months postoperatively. The carers completed similar questionnaires except for the UW-V4. Analysis of the patients’ data showed a serious deterioration in psychosocial and physical domains atone month postoperatively. However, the analysis of carers’ data showed a highly significant deterioration in anxiety and depression domains(p < 0.01), which remained low after three months. These findings highlight the need for psychological support not only for patients but also for their primary carers during the management of carcinoma of the head and neck

Porphyromonas gingivalis periodontal infection and its putative links with Alzheimer’s disease

Periodontal disease (PD) and Alzheimer’s disease (AD) are inflammatory conditions affecting the global adult population. In the pathogenesis of PD, subgingival complex bacterial biofilm induces inflammation that leads to connective tissue degradation and alveolar bone resorption around the teeth. In health, junctional epithelium seals the gingiva to the tooth enamel, thus preventing bacteria from entering the gingivae. Chronic PD involves major pathogens (Porphyromonas gingivalis, Treponema denticola and Tannerella forsythia) which have an immune armoury that can circumvent host’s immune surveillance to create, and maintain an inflammatory mediator rich, and toxic environment to grow and survive. The neurodegenerative condition, AD is characterised by poor memory and specific hallmark proteins; periodontal pathogens are increasingly being linked with this dementing condition. It is therefore becoming important to understand associations of periodontitis with relevance to late-onset AD. The aim of this review is to discuss the relevance of finding the keystone periodontal pathogen P. gingivalis in AD brains and its plausible contribution to the aetiological hypothesis of this dementing condition

Oral health and the Millennium and Sustainable Development Goals

The world is a complex and at times mystifying place. Sense and reason struggle for visibility among national terms of reference constructed around an individual nation’s needs, pride and (in some cases) survival. Embedded among these ‘instincts’ lurk the more menacing forces of power, influence and control. It is from such hybrid climates that the globally facing Millennium Development Goals (MDGs) and the succeeding Sustainable Development Goals (SDGs) emerged

Does the Use of 4% Articaine and 1:100,000 Adrenaline, Rather Than 2% Lidocaine and 1:100,000 Adrenaline, Increase the Risk of Nerve Damage When Administered for Inferior Alveolar Nerve Blocks in Patients Undergoing Local Anaesthesia for Dental Treatment? A Mini Systematic Review of The Literature

This mini systematic review seeks to analyse the available literature and determine if a 4% articaine solution poses a greater risk of inferior alveolar and/or lingual nerve damage compared to that of 2% lidocaine when administered for an inferior alveolar nerve block. After a mini systematic review search of the published literature, seven suitable studies were identified, one double blind random controlled trial (DBRCT) and six retrospective cohort studies. The DBRCT and 2 of the cohort studies concluded that 4% articaine poses no greater risk of nerve damage. The remaining 4 cohort studies suggested that caution should be exhibited when using a 4% local anaesthetic solution rather than a 2% solution. However, these studies also concluded that no evidence exists to explain the reasons for their results. The included articles present no conclusive evidence to suggest that 4% articaine causes more nerve damage than 2% lidocaine although some authors advise caution when using this agent. All studies conclude that further quality research is required and it is therefore suggested that dental practitioners exhibit caution when choosing to use 4% articaine in an inferior alveolar nerve block until further scientific research has been performe

Hyperkeratosis in potentially malignant disorder management – ‘guilty… until proven innocent!'

Why is clinician experience and judgment so important in the accurate assessment and effective management of newly presenting cases

Challenging the Clostridium botulinum toxin type A (BoNT/A) with a selection of microorganisms by culture methods and extended storage of used vials to assess the loss of sterility

In 2002, botulinum toxin type A (BoNT/A) was approved by the US Food and Drug Administration (FDA) for cosmetic use. However, there may be procedural differences between the ways in which a clinician handles, applies and stores the product compared to the suggested guidelines of the manufacturer for handling and storage. To this end vials (N = 12) of BoNT/A were tested for the incidence of microbial contamination followed by challenging the product with a selection of microorganisms by culture methods and by using a calcein release assay to contaminate multi-dose vials at the single concentration used for facial aesthetics. A culture, droplet method was used to count microorganisms challenged with the therapeutic product and to compare viability levels in appropriate controls as well as measuring their lytic properties via an existing cell-free system involving calcein release. Counts of test organisms within the droplets, with the product and the controls without the product were undertaken using Image J software. The result from the incidence of in-vial contamination was inconclusive. Bacterial levels between controls and product challenged groups demonstrated no differences in the growth of viable microorganisms following immediate contact (p = ≥ 0.05). The cell-free calcein release assay demonstrated differences at all time points for low levels of lysis in each case with bacterial lipid extract and were statistically significant (p = 0.011). Although these data appear to correlate with the minimum inhibitory concentration, the additives and vial integrity are also likely to contribute to the maintenance of BoNT/A sterility

Oral Inflammation, Tooth Loss, Risk Factors, and Association with Progression of Alzheimer’s Disease

Periodontitis is a polymicrobial chronic inflammatory disease of tooth-supporting tissues with bacterial etiology affecting all age groups, becoming chronic in a subgroup of older individuals. Periodontal pathogens Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola are implicated in the development of a number of inflammatory pathologies at remote organ sites, including Alzheimer’s disease (AD). The initial inflammatory hypothesis proposed that AD hallmark proteins were the main contributors of central nervous system (CNS) inflammation. This hypothesis is expanding to include the role of infections, lifestyle, and genetic and environmental factors in the pathogenesis of AD. Periodontal disease (PD) typifies a condition that encompasses all of the above factors including pathogenic bacteria. These bacteria not only are the source of low-grade, chronic infection and inflammation that follow daily episodes of bacteremia arising from everyday tasks such as brushing, flossing teeth, chewing food, and during dental procedures, but they also disseminate into the brain from closely related anatomical pathways. The long-term effect of inflammatory mediators, pathogens, and/or their virulence factors, reaching the brain systemically or otherwise would, over time, prime the brain’s own microglia in individuals who have inherent susceptibility traits. Such susceptibilities contribute to inadequate neutralization of invading agents, upon reaching the brain. This has the capacity to create a vicious cycle of sustained local inflammatory milieu resulting in the loss of cytoarchitectural integrity and vital neurons with subsequent loss of function (deterioration in memory). The possible pathways between PD and AD development are considered here, as well as environmental factors that may modulate/exacerbate AD symptoms

Periodontitis, microbiomes and their role in Alzheimer’s disease

As far back as the eighteenth and early nineteenth centuries, microbial infections were responsible for vast numbers of deaths. The trend reversed with the introduction of antibiotics coinciding with longer life. Increased life expectancy however, accompanied the emergence of age related chronic inflammatory states including the sporadic form of Alzheimer’s disease (AD). Taken together, the true challenge of retaining health into later years of life now appears to lie in delaying and/or preventing the progression of chronic inflammatory diseases, through identifying and influencing modifiable risk factors. Diverse pathogens, including periodontal bacteria have been associated with AD brains. Amyloid-beta (Aβ) hallmark protein of AD may be a consequence of infection, called upon due to its antimicrobial properties. Up to this moment in time, a lack of understanding and knowledge of a microbiome associated with AD brain has ensured that the role pathogens may play in this neurodegenerative disease remains unresolved. The oral microbiome embraces a range of diverse bacterial phylotypes, which especially in vulnerable individuals, will excite and perpetuate a range of inflammatory conditions, to a wide range of extra-oral body tissues and organs specific to their developing pathophysiology, including the brain. This offers the tantalizing opportunity that by controlling the oral-specific microbiome; clinicians may treat or prevent a range of chronic inflammatory diseases orally. Evolution has equipped the human host to combat infection/disease by providing an immune system, but Porphyromonas gingivalis and selective spirochetes, have developed immune avoidance strategies threatening the host-microbe homeostasis. It is clear from longitudinal monitoring of patients that chronic periodontitis contributes to declining cognition. The aim here is to discuss the contribution from opportunistic pathogens of the periodontal microbiome, and highlight the challenges, the host faces, when dealing with unresolvable oral infections that may lead to clinical manifestations that are characteristic for AD

Active invasion of Porphyromonas gingivalis and infection-induced complement activation in ApoE-/- mice brains

Periodontal disease is a polymicrobial inflammatory disease that leads to chronic systemic inflammation and direct infiltration of bacteria/bacterial components, which may contribute to the development of Alzheimer’s disease. ApoE-/- mice were orally infected (N = 12) with Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia and Fusobacterium nucleatum as mono- and polymicrobial infections. ApoE-/- mice were sacrificed following 12 and 24 weeks of chronic infection. Bacterial genomic DNA was isolated from all brain tissues except for the F. nucleatum mono-infected group. Polymerase chain reaction was performed using universal 16s rDNA primers and species- specific primer sets for each organism to determine whether the infecting pathogens accessed the brain. Sequencing amplification products confirmed the invasion of bacteria into the brain during infection. The innate immune responses were detected using antibodies against complement activation products of C3 convertase stage and the membrane attack complex. Molecular methods demonstrated that 6 out of 12 ApoE-/- mice brains contained P. gingivalis genomic DNA at 12 weeks (P = 0.006), and 9 out of 12 at 24 weeks of infection (P = 0.0001). Microglia in both infected and control groups demonstrated strong intracellular labeling with C3 and C9, due to on-going biosynthesis. Tthe pyramidal neurons of the hippocampus in 4 out of 12 infected mice brains demonstrated characteristic opsonization with C3 activation fragments (P = 0.032). These results show that the oral pathogen P. gingivalis was able to access the ApoE-/- mice brain and thereby contributed to complement activation with bystander neuronal injury

Can better management of periodontal disease delay the onset and progression of Alzheimer’s disease?

A risk factor relationship exists between periodontal disease and Alzheimer’s disease (AD) via tooth loss, and improved memory following dental intervention. This links the microbial contribution from indigenous oral periodontal pathogens to the manifestation of chronic conditions, such as AD. Here, we use Porphyromonas gingivalis infection to illustrate its effect on mental health. P. gingivalis infection, in its primary sub-gingival niche, can cause polymicrobial synergy and dysbiosis. Dysbiosis describes the residency of select commensals from the oral cavity following co-aggregation around the dominant keystone pathogen, such as P. gingivalis, to gain greater virulence. The initial process involves P. gingivalis disturbing neutrophil mediated innate immune responses in the healthy gingivae and then downregulating adaptive immune cell differentiation and development to invade, and subsequently, establish new dysbiotic bacterial communities. Immune responses affect the host in general and functionally via dietary adjustments caused by tooth loss. Studies from animals orally infected with P. gingivalis confirm this bacterium can transmigrate to distant organ sites (the brain) and contribute towards peripheral and intracerebral inflammation, and compromise vascular and microvascular integrity. In another study, P. gingivalis infection caused sleep pattern disturbances by altering glial cell light/dark molecular clock activity, and this, in turn, can affect the clearance of danger associated molecular patterns, such as amyloid-beta, via the glymphatic system. Since, P. gingivalis can transmigrate to the brain, and modulate organ-specific inflammatory innate and adaptive immune responses, this paper explores whether better management of indigenous periodontal bacteria could delay/prevent the onset and/or progression of dementia