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Background/Objectives: Osteoporosis causes a bone mass reduction and often determines acute and chronic pain. Understanding the biochemical and neurophysiological mechanisms behind this pain is crucial for developing new, effective rehabilitative and therapeutic approaches. This systematic review synthesizes recent advances in muscle–bone interactions and molecular pathways related to osteoporosis-associated pain. Methods: We carried out a systematic review including studies published from 2018 to 2024 using PubMed, Scopus, clinicaltrials.gov and Cochrane Library. The Cochrane Collaboration tool was used to assess bias risk. The review adhered to PRISMA guidelines and is registered with PROSPERO (CRD42024574456); Results: Thirteen studies were included. It emerged that osteoporosis causes progressive bone loss due to disruptions in biochemical processes and muscle–bone interactions. This condition is also closely associated with the development of pain, both acute and chronic. Key findings include the role of the miR-92a-3p/PTEN/AKT pathway and the impact of muscle–bone disconnection on bone health. Mechanotransduction is critical for bone maintenance. Effective pain management and rehabilitation strategies include physical therapy and physical exercise, yoga, Pilates, and cognitive behavioral therapy (CBT); they all improve pain relief and functional outcomes by enhancing muscle strength, flexibility, and balance. Pharmacological options such as NSAIDs, opioids, and new agents like SHR-1222, along with surgical interventions like percutaneous vertebroplasty, offer additional pain reduction, especially when included in individualized rehabilitation projects; Conclusions: This review highlights advancements in understanding osteoporotic pain mechanisms and identifies promising treatments. Integrating targeted therapies and rehabilitation strategies can enhance patients’ pain relief.

This work aimed to evaluate the potential of the nanosystems constituted by dopamine (DA) and the antioxidant Citicoline (CIT) co-loaded in solid lipid nanoparticles (SLNs) for intranasal administration in the treatment of Parkinson disease (PD). Such nanosystems, denoted as DA-CIT-SLNs, were designed according to the concept of multifunctional nanomedicine where multiple biological roles are combined into a single nanocarrier and prepared by the melt emulsification method employing the self-emulsifying Gelucire® 50/13 as lipid matrix. The resulting DA-CIT-SLNs were characterized regarding particle size, surface charge, encapsulation efficiency, morphology, and physical stability. Differential scanning calorimetry, FT-IR, and X ray diffraction studies were carried out to gain information on solid-state features, and in vitro release tests in simulated nasal fluid (SNF) were performed. Monitoring the particle size at two temperatures (4 °C and 37 °C), the size enlargement observed over the time at 37 °C was lower than that observed at 4 °C, even though at higher temperature, color changes occurred, indicative of possible neurotransmitter decomposition. Solid-state studies indicated a reduction in the crystallinity when DA and CIT are co-encapsulated in DA-CIT-SLNs. Interestingly, in vitro release studies in SNF indicated a sustained release of DA. Furthermore, DA-CIT SLNs displayed high cytocompatibility with both human nasal RPMI 2650 and neuronal SH-SY5Y cells. Furthermore, OxyBlot assay demonstrated considerable potential to assess the protective effect of antioxidant agents against oxidative cellular damage. Thus, such protective effect was shown by DA-CIT-SLNs, which constitute a promising formulation for PD application.