Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can be completely asymptomatic or, conversely, can cause coronavirus disease 2019 (COVID-19), for which the clinical outcomes range from mild upper airways symptoms to a severe disease with respiratory failure and a high fatality rate.¹ As of November 2020, more than 60 million people have been infected with SARS-CoV-2 worldwide, and more than 1.4 million people have died.²

Frailty is a highly prevalent condition in the elderly that has been increasingly considered as a crucial public health issue, due to the strict correlation with a higher risk of fragility fractures, hospitalization, and mortality. Among the age-related diseases, sarcopenia and dysphagia are two common pathological conditions in frail older people and could coexist leading to dehydration and malnutrition in these subjects. “Sarcopenic dysphagia” is a complex condition characterized by deglutition impairment due to the loss of mass and strength of swallowing muscles and might be also related to poor oral health status. Moreover, the aging process is strictly related to poor oral health status due to direct impairment of the immune system and wound healing and physical and cognitive impairment might indirectly influence older people’s ability to carry out adequate oral hygiene. Therefore, poor oral health might affect nutrient intake, leading to malnutrition and, consequently, to frailty. In this scenario, sarcopenia, dysphagia, and oral health are closely linked sharing common pathophysiological pathways, disabling sequelae, and frailty. Thus, the aim of the present comprehensive review is to describe the correlation among sarcopenic dysphagia, malnutrition, and oral frailty, characterizing their phenotypically overlapping features, to propose a comprehensive and effective management of elderly frail subjects.

Recently, 1α,25-dihydroxycholecalciferol (vitD) has received increasing interest for its effects on many tissues and organs other than bone. A number of experimental studies have shown that vitD may have an important role in modifying risk for cardiovascular disease. This study was planned to test the effects of vitD on endothelial nitric oxide (NO) production and to study the intracellular pathways leading to NO release. In human umbilical vein endothelial cells (HUVEC) cultures the effects of vitD on NO production and p38, Akt, ERK and eNOS phosphorylations were examined in absence or in presence of the NO synthase inhibitor L-NAME and protein kinases specific inhibitors SB203580, wortmannin and UO126. VitD caused a concentration-dependent increase in NO production. The maximum effect was observed at a concentration of 1 nM and the optimal time of stimulation was 1 min. Effects induced by vitD were abolished by L-NAME and by pre-treatment with protein kinases inhibitors. To verify the effective involvement of vitD receptor (VDR) in the action mechanism of vitD, experiments were repeated in presence of the specific VDR ligands ZK159222 and ZK191784. The results of this study demonstrate that vitD can induce a significant increase in endothelial NO production. VitD interaction with VDR caused the phosphorylation of p38, AKT and ERK leading to eNOS activation.

Temporomandibular disorders (TMD) are a group of musculoskeletal diseases affecting masticatory muscles and temporomandibular joints (TMJ). In this context, the chronic TMD could be considered as a condition with chronic primary orofacial pain, presenting as myofascial TMD pain or TMJ arthralgia. In this context, myogenous TMD may present overlapping features with other disorders, such as fibromyalgia and primary headaches, characterized by chronic primary pain related to dysfunction of the central nervous system (CNS), probably through the central sensitization. This phenomenon could be defined as an amplified response of the CNS to sensory stimuli and peripheral nociceptive, characterized by hyperexcitability in the dorsal horn neurons in the spinal cord, which ascend through the spinothalamic tract. The main objectives of the management of TMD patients are: decreasing pain, increasing TMJ function, and reducing the reflex masticatory muscle spasm/pain. The first-line treatments are physical therapy, pharmacological drugs, occlusal splints, laser therapy, extracorporeal shockwave therapy, transcutaneous electrical nerve stimulation, and oxygen–ozone therapy. Although all these therapeutic approaches were shown to have a positive impact on the central sensitization of TMD pain, there is still no agreement on this topic in the scientific literature. Thus, in this comprehensive review, we aimed at evaluating the evidence on pain management and rehabilitation for the central sensitization in TMD patients.

Alterations in the tumor suppressor phosphatase and tensin homolog (PTEN) occur in a substantial proportion of solid tumors. These events drive tumorigenesis and tumor progression. Given its central role as a downregulator of the phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway, PTEN is deeply involved in cell growth, proliferation, and survival. This gene is also implicated in the modulation of the DNA damage response and in tumor immune microenvironment modeling. Despite the actionability of PTEN alterations, their role as biomarkers remains controversial in clinical practice. To date, there is still a substantial lack of validated guidelines and/or recommendations for PTEN testing. Here, we provide an update on the current state of knowledge on biologic and genetic alterations of PTEN across the most frequent solid tumors, as well as on their actual and/or possible clinical applications. We focus on possible tailored schemes for cancer patients’ clinical management, including risk assessment, diagnosis, prognostication, and treatment.

Over the last few decades, studies on the oral microbiome have increased awareness that the balance between the host and the microbial species that coexist in it is essential for oral health at all stages of life. However, this balance is extremely difficult to maintain, and many factors can disrupt it: general eating habits, sugar consumption, tobacco smoking, oral hygiene, and use of antibiotics and other antimicrobials. It is now known that alterations in the oral microbiota are responsible for developing and promoting many oral diseases, including periodontal disease. In this context, diet is an area for further investigation as it has been observed that the intake of particular foods, such as farmed animal meat, dairy products, refined vegetable oils, and processed cereals, affects the composition of the microbiota, leading to an increased representation of acid-producing and acid-tolerant organisms and periodontal pathogens. However, little is known about the influence of diet on the oral microbiome and the creation of a suitable microenvironment for the development of periodontal disease. The aim of the present study is to evaluate current knowledge on the role of diet in the oral dysbiosis underlying periodontal disease.