Periodontitis is a chronic inflammatory disease caused by the presence of a bacterial biofilm known as dental plaque. This biofilm affects the supporting apparatus of the teeth, especially the periodontal ligaments and the bone surrounding the teeth. Periodontal disease and diabetes seem to be interrelated and in a bidirectional relationship, and have been increasingly studied in recent decades. For example, diabetes mellitus has a detrimental effect on periodontal disease, increasing its prevalence, extent, and severity. In turn, periodontitis negatively affects glycemic control and the course of diabetes. This review aims to present the most recently discovered factors that contribute to the pathogenesis, therapy, and prophylaxis of these two diseases. Specifically, the article focuses on microvascular complications, oral microbiota, pro- and anti-inflammatory factors in diabetes, and periodontal disease. As presented in this review, these two diseases require specific/ complementary therapeutic solutions when they occur in association, with new clinical trials and epidemiological research being necessary for better control of this interdependent pathogenic topic.

Background/Objectives: Type 2 diabetes mellitus (T2DM) has been evaluated through a glucocentric model centered on hyperglycemia, glycated haemoglobin (HbA1c) targets, and complications. However, obesity-associated T2DM reflects a broader metabolic ecosystem in which glycemic control interacts with adiposity, inflammation, muscle function, renal stability, and treatment mechanisms. Therapeutic response may be better captured through patient-level responder phenotypes than through mean changes in isolated outcomes. We aimed to determine, in adults with obesity-associated T2DM maintained on stable 12-month metformin-based regimens, the distribution of concordant versus discordant glycemic–adiposity response phenotypes and the frequency of high multidimensional response, and to describe how these phenotypes were distributed across treatment classes. Methods: This secondary patient-level analysis used a real-world cohort from a Bucharest tertiary diabetes center. Of 291 screened adults, 166 completed 12-month follow-up without treatment change. Regimens included metformin alone or combined with sulfonylurea, DPP-4 inhibitor, SGLT2 inhibitor, GLP-1 receptor agonist, or insulin. Responses were defined as HbA1c reduction ≥ 0.5 percentage points, fat mass reduction ≥ 5%, hs-CRP reduction ≥ 20%, and handgrip strength decline ≤ 1 kg. Primary phenotypes and a 0–4 multidimensional score were derived. Results: Mean age was 59.7 ± 13.0 years, BMI 36.3 ± 4.4 kg/m², and baseline HbA1c 8.9 ± 1.0%. Glycemic–adiposity, glycemic-only, adiposity-only, and low/non-response phenotypes occurred in 49 (29.5%), 88 (53.0%), 9 (5.4%), and 20 (12.0%) patients, respectively. A high multidimensional response occurred in 78 (47.0%), and complete response in 25 (15.1%). GLP-1 receptor agonists showed the most consistent concordant glycemic–adiposity response, whereas insulin was predominantly glycemic-only. Conclusions: In obesity-associated T2DM, therapeutic response was heterogeneous and frequently discordant across metabolic domains. Patient-level responder phenotyping may complement conventional HbA1c-centered evaluation by identifying response quality across glycemic, adiposity, inflammatory, and functional dimensions. This approach may support more individualized diagnostic interpretation and treatment optimization in real-world diabetes care.

Background and Objectives: The management of type 2 diabetes (T2D) extends beyond glycemic control, requiring a more global strategy that includes optimization of body composition, even more so in the context of sarcopenia and visceral adiposity, as they contribute to poor outcomes. Past reviews have typically been focused on weight reduction or glycemic effectiveness, with limited inclusion of new therapies’ effects on muscle and fat distribution. In addition, the emergence of incretin-based therapies and dual agonists such as tirzepatide requires an updated synthesis of their impacts on body composition. This review attempts to bridge the gap by taking a systematic approach to how current blood-glucose lowering therapies affect lean body mass, fat mass, and the risk of sarcopenia in T2D patients. Materials and Methods: Between January 2015 and March 2025, we conducted a narrative review by searching the PubMed, Scopus, and Web of Science databases for English-language articles. The keywords were combinations of the following: “type 2 diabetes,” “lean body mass,” “fat mass,” “body composition,” “sarcopenia,” “GLP-1 receptor agonists,” “SGLT2 inhibitors,” “tirzepatide,” and “antidiabetic pharmacotherapy.” Reference lists were searched manually as well. The highest precedence was assigned to studies that aimed at adult type 2 diabetic subjects and reported body composition results. Inclusion criteria for studies were: (1) type 2 diabetic mellitus adult patients and (2) reporting measures of body composition (e.g., lean body mass, fat mass, or muscle function). We prioritized randomized controlled trials and large observational studies and excluded mixed diabetic populations, non-pharmacological interventions only, and poor reporting of body composition. Results: Metformin was widely found to be weight-neutral with minimal effects on muscle mass. Insulin therapy, being an anabolic hormone, often leads to fat mass accumulation and increases the risk of sarcopenic obesity. Incretin-based therapies induced substantial weight loss, mostly from fat mass. Notable results were observed in studies with tirzepatide, demonstrating superior reduction not only in fat mass, but also in visceral fat. Sodium-glucose cotransporter 2 inhibitors (SGLT2 inhibitors) promote fat loss but are associated with a small yet significant decrease in lean muscle mass. Conclusions: Blood-glucose lowering therapies demonstrated clinically relevant effects on body composition. Treatment should be personalized, balancing glycemic control, cardiovascular, and renal benefits, together with optimal impact on muscle mass along with glycemic, cardiovascular, and renal benefits.

Post-partum depression is one of the most severe types of depression and can be developed at any age, no matter of cultural of social status. Objectives. To determine the factors associated with the psychological impact of pregnancy and to emphasize the psychological and psychiatric risks after giving birth for a woman. Materials and Methods. The study enrolled 35 patients diagnosed with postpartum depression that have been hospitalized in a tertiary-care center for psychiatric disorders between 2016 and 2020. Data were collected from patients’ observation charts. Results. The incidence of postpartum depression is higher in the age range 30-45 years old for primiparous women who are from urban areas, unemployed and not integrated in a family (unbalanced families or single parents), with medium level of education (high school) and alcohol addiction. One of 35 patients committed infanticide. Conclusions. Even if the postpartum depression is known worldwide it is still underdiagnosed, with certain factors concurring to that. Postpartum depression requires the identification of risk conditions in pregnant women and individualized therapy in a patient-centered, holistic manner.

Background/Objectives: In obesity-associated type 2 diabetes (T2DM), therapeutic benefit increasingly requires assessment of not only HbA1c and total body weight, but also the composition and functional quality of weight change. We evaluated a myoprotective fat-loss phenotype, defined as a reduction in adiposity accompanied by preservation of lean mass and handgrip strength. Methods: This secondary patient-level analysis included 166 adults with T2DM who completed 12 months of follow-up without changing treatment in a real-world tertiary diabetes cohort. Patients received metformin alone or metformin combined with a sulfonylurea, a DPP-4 inhibitor, an SGLT2 inhibitor, a GLP-1 receptor agonist, or insulin. Body composition was assessed by bioimpedance and muscle function by handgrip dynamometry. The primary phenotype required a reduction in fat mass ≥5%, a loss of lean mass <3%, and a decrease in handgrip ≤1 kg. Phenotype distributions were compared between treatment groups; patient-level associations and adjusted contrasts were explored using correlation analyses and baseline-adjusted regression models with robust HC3 standard errors. Results: Fat-mass reduction ≥5% occurred in 58/166 patients (34.9%), lean-mass preservation in 129/166 (77.7%), and handgrip preservation in 143/166 (86.1%). The complete myoprotective phenotype was present in 35/166 patients (21.1%) and differed significantly across treatment groups (χ² = 131.58; permutation p < 0.0001). It was most frequent in the GLP-1 receptor agonist group (13/23; 56.5%) and the SGLT2 inhibitor group (12/25; 48.0%), less frequent with metformin monotherapy (9/46; 19.6%) and DPP-4 inhibitors (1/17; 5.9%), and absent in the sulfonylurea and insulin groups. GLP-1 receptor agonists showed the greatest crude fat-mass loss, whereas lean-mass loss, skeletal-muscle-mass change, and handgrip change did not differ significantly across groups after false-discovery-rate correction. Conclusions: Myoprotective fat-loss phenotypes can be identified in obesity-associated T2DM using body composition and handgrip measures. These observational findings support the assessment of the quality, not just the magnitude, of weight loss in diabetes care and require validation in larger prospective studies.