In the context of thermal injury, local tissue integrity and systemic homeostasis are compromised, often resulting in delayed healing, infections, and disturbances of the skin and intestinal microbial balance. Despite several reviews addressing probiotics in wound healing, none has specifically focused on their role in thermal injuries and burn-associated pathophysiology. This review uniquely integrates evidence on the gut–skin axis, postbiotic innovations, and regenerative perspectives tailored to burn care. We conducted a critical synthesis of recent preclinical and clinical trials evaluating the use of probiotics and their derivatives to promote tissue regeneration following burn injury. Previous reviews have addressed probiotics in general wound repair, but the present synthesis advances the field by bridging mechanistic insights (immune modulation, angiogenesis, microbiome restoration) with translational evidence in burn patients, offering a framework for personalized regenerative approaches. Based on a structured review of the literature—including in vitro models, animal experiments, and randomized trials with topical, enteral, and systemic administration of probiotic—we identified four main mechanisms of action: modulation of the immune response by balancing cytokines and polarization of T lymphocytes; stimulation of tissue repair by increasing the proliferation of keratinocytes and fibroblasts, increased collagen synthesis, and induction of angiogenesis; direct antimicrobial activity against biofilms and multiresistant pathogens; and the restoration of eubiosis with the improvement of the function of epithelial barriers. While these findings endorse the adjunctive use of probiotics in burn management, large multicenter trials are required to standardize strains, dosages, and formulations before their routine clinical adoption.

Background: Angiogenesis, the formation of new blood vessels from pre-existing ones, plays a pivotal role in wound healing, particularly in surgical contexts. Methods and results: However, this process can be significantly impaired in patients with childhood obesity, resulting in delayed healing and additional complications. The biological process of wound healing is complex, involving angiogenesis, cell proliferation, inflammation, and tissue remodeling. This review aims to explore recent advancements in research on angiogenesis in surgical wounds in patients with childhood obesity, with a focus on growth factors, inflammation, microcirculation, and innovative therapeutic strategies. Conclusions: It highlights therapeutic approaches such as the administration of growth factors and the application of biomaterials to enhance angiogenesis.

Cerebral ischemia represents a major mortality and disability cause; oxidative stress is the main intensifier mechanism of excitotoxicity, neuroinflammation, blood–brain barrier failure, and neuronal loss; under these circumstances, firm, mechanism-anchored neuroprotection is an absolute necessity. The work includes a exhaustive, PRISMA (Preferred reporting items for systematic review and meta-analysis)-adherent presentation of the effects of antioxidant peptides and small molecules on tissues, unifying disparate readouts into a coherent tissue-level narrative. A systematic interrogation was performed across major databases over a prespecified interval, applying transparent eligibility criteria to studies that quantified canonical endpoints—infarct volume, neuronal integrity (NeuN/MAP2), apoptosis (TUNEL/cleaved caspase-3), gliosis (GFAP/Iba1), and ultrastructural preservation. The evidence coalesces around a strikingly consistent signal: antioxidant strategies converge on smaller infarcts, robust preservation of neuronal markers, attenuation of apoptotic burden, dampened astroglial–microglial reactivity, and stabilization of mitochondrial and axonal architecture—patterns that align with antioxidative, anti-apoptotic, anti-inflammatory, and ferroptosis-modulating mechanisms. While early clinical data echo these benefits, translation is tempered by heterogeneity in models, timing and dosing windows, and outcome batteries. By consolidating the histological landscape and pinpointing where effects are durable versus contingent, this work elevates antioxidant peptide and small-molecule neuroprotection from promising fragments to an integrated framework and sets an actionable agenda—standardized histological endpoints, protocol harmonization, head-to-head comparisons of peptide versus small-molecule strategies, and adequately powered randomized trials embedded with mechanistic biomarkers to decisively test efficacy and accelerate clinical adoption.

Background and Objectives: Rosacea is a chronic inflammatory dermatosis with a complex pathophysiology that continues to challenge effective long-term disease management. Rosacea is characterized by immune dysregulation, oxidative stress, neurovascular dysfunction, and impaired epidermal barrier integrity, while current therapeutic options remain limited. Hippophae rhamnoides (sea buckthorn) is a phytochemically rich medicinal plant with reported anti-inflammatory and dermo-reparative properties. Materials and Methods: A systematic literature review was conducted following PRISMA guidelines using the PubMed database. Studies published from 2020 onward evaluating sea buckthorn extracts, oils, or isolate bioactive compounds in the in vitro, in vivo, and limited clinical contexts were included, with emphasis on rosacea relevant mechanisms. Results: Twenty-six studies show that sea buckthorn compounds modulate inflammation, oxidative stress, vascular and immune responses, and barrier function in preclinical models. They consistently reduce pro-inflammatory mediators, improve barrier integrity, and attenuate immune or vascular activation, suggesting potential benefits for inflammatory skin disorders such as rosacea. Conclusions: Hippophae rhamnoides shows promising anti-inflammatory and skin-repairing effects that may benefit patients with rosacea. However, most evidence comes from preclinical studies, and clinical data specifically for rosacea are limited. Well-designed clinical trials are needed to confirm its effectiveness in treating this condition.

Background: Patients with diabetes mellitus exhibit increased susceptibility to peri-implant inflammation and implant failure due to systemic metabolic dysfunction, impaired immunity, and delayed tissue healing. The oral microbiome is increasingly recognized as a key intermediary in these pathogenic processes. Aims: This review aims to systematically evaluate the available literature examining the relationships among the oral microbiome, biomaterial biocompatibility, and inflammatory changes in peri-prosthetic tissues in insulin-dependent diabetic patients. Methods: A systematic search of PubMed and Scopus databases identified studies published between January 2000 and July 2025. Eligible studies (25 in total) included clinical, histological, microbiological, or immunohistochemical investigations involving diabetic patients rehabilitated with dental implants or prostheses. Study selection and reporting followed PRISMA 2020 guidelines. Results: Diabetic cohorts showed consistent microbial alterations, including a higher relative abundance of periopathogenic species (P. gingivalis, T. forsythia, and F. nucleatum), lower microbial diversity, and greater biofilm-forming potential. Histological analyses frequently described increased inflammatory infiltrates, higher cytokine expression, and reduced soft-tissue integration. Biomaterial surface characteristics were also associated with differences in microbial adhesion, while hyperglycemia was linked to microbial and host-response patterns suggestive of greater pathogenicity and inflammation. Collectively, these findings suggest that diabetes-associated dysbiosis may be associated with increased peri-implant inflammatory changes and altered peri-implant homeostasis. Conclusions: The oral microbiome may be involved in inflammatory activity and biocompatibility at the tissue–implant interface in diabetic patients. A better understanding of host–microbe–material interactions may support risk assessment and help inform future personalized management strategies, such as targeted antimicrobial approaches, probiotic modulation, and biomaterial surface optimization, although these implications should be interpreted cautiously given the predominantly observational and heterogeneous nature of the available evidence.

Pigment disorders of both aging skin and retina involve many common mechanisms. A better understanding of such mechanisms might lead to effective prevention and noninvasive therapy strategies applicable to both locations of pigmentary disorders. The direct consequence of such pigmentary disorders involving the retinal tissue generates age-related macular degeneration (AMD), the leading cause of vision loss in the elderly, which occurs as a progressive loss of macular pigments. Oxidative stress on retinal pigment is nowadays exacerbated by environmental factors such as chronic ultraviolet (UV) exposure, pollution, toxic heavy metal accumulation, and amplified by climate change. Increased risks of damaging effects urge proactive preventive strategies and therapies. Nutritional antioxidant supplementation has emerged as a key preventive approach. Clinical studies in AMD patients indicate that long-term Xanthophyll carotenoid supplementation can slow the progression of degeneration and vision loss. Beyond these, a variety of plant-derived supplements have demonstrated significant in vitro/in vivo antioxidative activity, with protective anti-aging effects. This comprehensive paradigm, linking antioxidative nutrition, environmental risk mitigation, and medical therapies, exemplifies a modern translational strategy to reduce oxidative damage and improve outcomes in retinal aging pigment disorders.