An expanding body of research asserts that the gut microbiota has a role in bone metabolism and the pathogenesis of osteoporosis. This review considers the human gut microbiota composition and its role in osteoclastogenesis and the bone healing process, specifically in the case of osteoporosis. Although the natural physiologic processes of bone healing and the pathogenesis of osteoporosis and bone disease are now relatively well known, recent literature suggests that a healthy microbiome is tied to bone homeostasis. Nevertheless, the mechanism underlying this connection is still somewhat enigmatic. Based on the literature, a relationship between the microbiome, osteoblasts, osteoclasts, and receptor activator of nuclear factor-kappa-Β ligand (RANKL) is contemplated and explored in this review. Studies have proposed various mechanisms of gut microbiome interaction with osteoclastogenesis and bone health, including micro-RNA, insulin-like growth factor 1, and immune system mediation. However, alterations to the gut microbiome secondary to pharmaceutical and surgical interventions cannot be discounted and are discussed in the context of clinical therapeutic consideration. The literature on probiotics and their mechanisms of action is examined in the context of bone healing. The known and hypothesized interactions of common osteoporosis drugs and the human gut microbiome are examined. Since dysbiosis in the gut microbiota can function as a biomarker of bone metabolic activity, it may also be a pharmacological and nutraceutical (i.e., pre- and probiotics) therapeutic target to promote bone homeostasis.

While the gut microbiome is composed of numerous bacteria, specific bacteria within the gut may play a significant role in carcinogenesis, progression, and metastasis of colorectal carcinoma (CRC). Certain microbial species are known to be associated with specific cancers; however, the interrelationship between bacteria and metastasis is still enigmatic. Mounting evidence suggests that bacteria participate in cancer organotropism during solid tumor metastasis. A critical review of the literature was conducted to better characterize what is known about bacteria populating a distant site and whether a tumor depends upon the same microenvironment during or after metastasis. The processes of carcinogenesis, tumor growth and metastatic spread in the setting of bacterial infection were examined in detail. The literature was scrutinized to discover the role of the lymphatic and venous systems in tumor metastasis and how microbes affect these processes. Some bacteria have a potent ability to enhance epithelial–mesenchymal transition, a critical step in the metastatic cascade. Bacteria also can modify the microenvironment and the local immune profile at a metastatic site. Early targeted antibiotic therapy should be further investigated as a measure to prevent metastatic spread in the setting of bacterial infection.

The teach-back method is a valuable communication tool that can be employed to improve patient safety and shared decision-making. Its utility in patient care has been studied extensively in many areas of clinical medicine. However, the literature on the use of teach-back in surgical patient education and informed consent is limited. Additionally, there is some ambiguity about the functional definition and performance of the teach-back method in the literature, consequently rendering this valuable tool an enigma. This review examines the current standards and ethics of preoperative informed consent and provides a concise, actionable definition of teach-back. The manner in which teach-back has been implemented in medicine and surgery is then examined in detail. Studies analyzing the use of teach-back in medicine have demonstrated its effectiveness and benefit to patient care. Further study on the use of teach-back to improve preoperative informed consent is supported by the few preliminary trials showing a positive effect after implementing the teach-back method in critical patient interactions.

Adrenal incidentalomas are incidentally discovered adrenal masses greater than one centimeter in diameter. An association between insulin resistance and adrenal incidentalomas has been established. However, the pathophysiological link between these two conditions remains incompletely characterized. This review examines the literature on the interrelationship between insulin resistance and adrenal masses, their subtypes, and related pathophysiology. Some studies show that functional and non-functional adrenal masses elicit systemic insulin resistance, whereas others conclude the inverse. Insulin resistance, hyperinsulinemia, and the anabolic effects on adrenal gland tissue, which have insulin and insulin-like growth factor-1 receptors, offer possible pathophysiological links. Conversely, autonomous adrenal cortisol secretion generates visceral fat accumulation and insulin resistance. Further investigation into the mechanisms and timing of these two pathologies as they relate to one another is needed and could be valuable in the prevention, detection, and treatment of both conditions.

Gastric cancer metastasis is a process in which the tumor microenvironment may carry significant influence. Helicobacter pylori (H. pylori) infection is well-established as a contributor to gastric carcinoma. However, the role that these bacteria and others may play in gastric carcinoma metastasis is a current focus of study. A review of the literature was conducted to elucidate the process by which gastric adenocarcinoma metastasizes, including its ability to utilize both the lymphatic system and the venous system to disseminate. Studies that investigate the tumor microenvironment at both the primary and secondary sites were assessed in detail. H. pylori and Mycoplasma hyorhinis (M. hyorhinis) were found to be important drivers of the pathogenesis of gastric adenocarcinoma by modifying various steps in cell metastasis, including epithelial–mesenchymal transition, cell migration, and cell invasion. H. pylori is also a known driver of MALT lymphoma, which is often reversible simply with the eradication of infection. M. hyorhinis has been implicated in gastric neoplasia via β-catenin stabilization and subsequent activation of the WNT-signaling pathway, promoting gastric cancer cell motility and inciting cancer progression. Fusobacterium nucleatum (F. nucleatum) and its association with worse prognosis in diffuse-type gastric adenocarcinoma are also reviewed. Recognition of the roles that bacteria play within the metastatic cascade is vital in gastrointestinal adenocarcinoma treatment and potential reoccurrence. Further investigation is needed to establish potential treatment for metastatic gastric carcinoma by targeting the tumor microenvironment.

The implications of recent discoveries pertaining to immune-mediated disease and the human gut microbiome are vast. In a symbiotic relationship, the immune system modulates the maintenance of host-microbe normobiosis, and the gut microbiome plays a critical role in developing and maintaining the host's innate and adaptive immune systems. The cutting edge of microbiome research and personalized medicine targets the clinical application and exploitation of gut microbiota modulation in the setting of specific diseases. For example, prebiotic/probiotic supplementation, microbiome enhancing diets, and fecal microbiota transplant have been studied as potential ameliorative supplemental interventions to combined antiretroviral therapy (cART) in human immunodeficiency virus-positive (HIV+) individuals. Furthermore, recent evidence shows a positive correlation between improved CD4+ cell counts in HIV+ individuals and improved gut microbiota profile after cART. We supplement this finding with data and supporting evidence from recent studies to aid in the clinical application of these findings in this commentary. Preliminary data support the consideration of the gut microbiota in the proactive management of HIV-associated comorbidities.

Cadaveric dissection has long been a central component of medical school curricula in both allopathic and osteopathic training. However, presumptive and lengthy dissection instructions in commonly used laboratory guides are among the limiting factors in foundational dissection experiences, causing a steep learning curve. This educational study aims to produce a more precise and practical dissection guide for the historically difficult dissection of the human head; including disarticulation, bisection, and the dissection of the pharynx & larynx. Hypothesized to provide memory and learning anchors due to ease of association, osteopathic correlations and anatomical considerations are provided throughout the guide, particularly in the disarticulation process. In addition, the guide aims to allow a student to succeed on their first attempt at dissecting by providing students’ perspectives on the procedures involved; including photos, pitfalls, and tips. Clinical correlations are also provided throughout. Medical students are encouraged to begin reasoning from their understanding of anatomy, and this dissection manual is intended to guide them in doing so.

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