Life Sciences Student Journal

Microenvironmental Control of Dental Implant Osseointegration

Mahdis Nesabiand, Sirus Safaee, Mohammad Reza Nourani — Wed, 18 Feb 2026 00:00:00 +0000

The dental implant interface (DII) constitutes a highly specialized and dynamic microenvironment that emerges immediately following implant placement and governs the biological success or failure of osseointegration. Distinct from native bone healing, the DII is shaped by the presence of a permanent foreign biomaterial, surgical trauma, host immune responses, and evolving mechanical stimuli. This review synthesizes contemporary evidence from periodontology, molecular biology, and biomaterials science to provide an integrated, phase-dependent framework of repair and osseointegration at the DII. We delineate the temporal progression of healing into hemostatic, inflammatory, proliferative, and remodeling phases, highlighting the molecular signaling networks, cellular dynamics, and mechanobiological cues that regulate each stage. Particular emphasis is placed on osteoimmunological mechanisms, including macrophage polarization and immune–bone crosstalk, as critical determinants of regenerative versus fibrotic healing outcomes. Additionally, the role of biochemical gradients, physicochemical conditions, and implant surface properties in directing protein adsorption, cell fate decisions, angiogenesis, and soft tissue integration is discussed. Translational implications for implant surface design, surgical protocols, and loading strategies are explored, underscoring the shift toward biologically intelligent and immunomodulatory implant systems. Finally, emerging approaches such as single-cell and spatial omics are presented as future tools to enable personalized implant therapy and improve long-term peri-implant tissue stability.

Three Lines of Defense: Macrophage Subset Compartmentalization in Salmonella-Infected Peyer's Patches

Seyed Ali Mirhosseini, Mohammad Reza Nourani — Wed, 18 Feb 2026 00:00:00 +0000

Background: Salmonella enterica serovar Typhimurium is a major enteric pathogen that invades the host via M cells overlying Peyer's patches. Macrophages are critical for host defense, yet the anatomical distribution of distinct macrophage subsets within Peyer's patches during active infection remains incompletely characterized.

Methods: Female C57BL/6 mice were orally infected with Salmonella Typhimurium strain SL1344 following streptomycin pretreatment. At 7 days post-infection, cecal Peyer's patches were examined macroscopically and by immunohistochemistry using antibodies against F4/80, Moma1, and Moma2.

Results: Infected mice exhibited marked cecal hyperemia, wall thickening, and enlarged Peyer's patches. F4/80⁺ macrophages densely accumulated in the subepithelial dome (SED) and were also observed in follicular periphery and perivascular areas. Moma1⁺ cells were sharply delineated around B-cell follicles and vessels, with no staining in SED or interfollicular regions (IFR). Moma2⁺ macrophages were widely distributed outside follicles, with highest density in IFR and around high endothelial venules.

Conclusion: Oral Salmonella infection induces compartmentalized redistribution of macrophage subsets in Peyer's patches. F4/80⁺ cells serve as first-line phagocytes at the bacterial entry site, Moma1⁺ cells function as barrier sentinels, and Moma2⁺ cells localize to T-cell zones for antigen presentation. This functional topography informs mucosal vaccine design.

Early Photoreceptor Apoptosis and Microglial Response in Light-Damaged Mouse Retina

Hanieh Shojaee, Mohammad Reza Nourani — Fri, 20 Feb 2026 00:00:00 +0000

Background: The retina, as part of the central nervous system, has limited capacity for self-repair following injury. Light-induced retinopathy serves as a valuable model for studying retinal degeneration, but the early events following photic injury remain incompletely characterized.

Objective: This study investigated the temporal and spatial relationship between photoreceptor apoptosis and macrophage response during the first three days after light-induced retinal damage.

Methods: Adult BALB/c mice were exposed to intense cool white fluorescent light (3,500-7,000 lux) for 7 hours and sacrificed at 1, 2, and 3 days post-injury. Retinal sections were examined using toluidine blue staining for morphology, TUNEL assay for apoptotic cells, and F4/80 immunohistochemistry for macrophages/microglia.

Results: Progressive outer nuclear layer (ONL) thinning was observed, with near-complete photoreceptor loss by day three. TUNEL-positive apoptotic cells appeared exclusively in the ONL, peaking at day two and declining by day three. F4/80-positive cells transformed from ramified to amoeboid morphology, increased in number, and migrated to the ONL, with peak accumulation at days two to three.

Conclusion: Photoreceptor apoptosis peaks at 48 hours post-injury, closely followed by microglial activation and recruitment to the site of damage. This temporal sequence confirms a direct relationship between cell death and inflammatory response, identifying the first 48 hours as a critical therapeutic window for intervention in retinal degenerative diseases.

From Acute Exposure to Chronic Disease: Deciphering the Molecular and microRNA Signature of Sulfur Mustard Toxicity

shahram parvin, Mohammad Reza Nourani — Wed, 18 Feb 2026 00:00:00 +0000

Sulfur mustard (SM) is a potent alkylating agent that causes severe acute injuries to the skin, eyes, and respiratory tract. Its devastating legacy extends decades beyond initial exposure, manifesting as chronic conditions like "mustard lung," skin lesions, and pulmonary fibrosis in survivors of the Iraq war against Iran. The molecular pathogenesis linking acute alkylation damage to these progressive disorders remains a critical enigma.

This review synthesizes contemporary research to map this complex trajectory, detailing the initial cascade of DNA damage, oxidative stress, and necroptosis, followed by sustained inflammation and pro-fibrotic signaling. We particularly focus on the central role of TGF-β/Smad and Trefoil Factor Family 1 (TFF1) in airway remodeling. A major emphasis is placed on epigenetic dysregulation, specifically microRNAs (miRNAs). We consolidate evidence identifying specific miRNAs such as upregulated miR-21 in skin fibrosis and dysregulated urinary miR-9 and miR-143 as promising diagnostic biomarkers. By integrating molecular pathogenesis with cutting-edge biomarker discovery, this review provides a framework for understanding SM's long-term toxicity and highlights potential tools to mitigate the enduring burden on exposed veterans.

Postbiotics as Modulators of Apoptotic and Metastatic Pathways in Colorectal Cancer: Insights from HT-29 Cell Responses

Hiva safaei — Sat, 06 Dec 2025 00:00:00 +0000

Colorectal cancer is one of the leading causes of cancer-related morbidity and mortality worldwide, and its incidence is strongly influenced by diet, lifestyle, chronic inflammation, and the composition of the gut microbiota.[1–4] Increasing evidence suggests that microbial dysbiosis contributes to tumor initiation and progression through altered metabolite production, impaired barrier function, and activation of oncogenic signaling pathways such as Wnt/β-catenin, NF-κB, MAPK/ERK, and STAT3.[3,5,6,14,19] In parallel, interest has grown in microbiota-centered interventions, particularly probiotics, prebiotics, synbiotics, and more recently postbiotics, which are defined as non-viable microbial cells, components, or metabolites that exert health-promoting effects in the host.[3,7–10] Postbiotics are attractive because they are stable, safe for immunocompromised patients, and easier to standardize than live probiotics, while still retaining potent immunomodulatory, anti-inflammatory, and anticancer activities.[7–13,21,26] Experimental and review data indicate that postbiotics can inhibit CRC cell growth, induce apoptosis, modulate the cell cycle, and regulate metastasis-associated genes and pathways, including RSPO2, NGF, MMP7, and mitochondrial apoptosis regulators such as Bax, Bcl-2, and caspase-3.[10–13,16,17,20] In particular, postbiotics derived from Bifidobacterium breve and Lactobacillus rhamnosus have shown promising effects in HT-29 colorectal cancer cells, where they promote apoptosis and attenuate pro-metastatic gene expression.[10,20] This review summarizes current knowledge on the relationship between the gut microbiota and CRC, defines and contextualizes postbiotics, explores their molecular mechanisms in carcinogenesis with a focus on CRC, and discusses the translational and clinical potential of postbiotics as complementary tools in CRC prevention and management.[3,7,11–13,18,26–28]

Collagen-Based Bioactive Materials for Tissue Engineering: From Fundamental Properties to Clinical Translation and Future Horizons

Soheila Naderi, Mohadeseh Valizadeh, Sirus Safaee, Mohammad Reza Nourani — Sat, 21 Feb 2026 00:00:00 +0000

Collagen, the predominant structural protein in the extracellular matrix (ECM), has gained significant attention as a natural bioactive material for tissue engineering. Its intrinsic biocompatibility, biodegradability, and low immunogenicity, together with cell-recognition motifs such as Arg-Gly -Asp (RGD), enable specific interactions with integrins and growth factors that regulate cell adhesion, migration, and differentiation. Recent progress in collagen-based scaffold design including hydrogels, sponges, nanofibers, and composite matrices, has expanded its use across multiple tissue systems such as bone, cartilage, skin, vascular, corneal, and neural regeneration. Incorporation of synthetic polymers (e.g., polycaprolactone, polylactic acid, polyethylene glycol) and inorganic bioactives (e.g., hydroxyapatite, bioactive glass, silica nanoparticles) has enhanced the mechanical performance and degradation control of collagen-based constructs, addressing the limitations of native collagen. Nevertheless, batch variability, rapid enzymatic degradation, and limited long-term stability continue to constrain clinical applications. Emerging directions, including recombinant and marine-derived collagens, nanocomposite reinforcement, gene-activated matrices, and 3D/4D bioprinting technologies, are opening new pathways toward personalized, scalable, and immunocompatible tissue-engineered products. This review synthesizes two decades of progress, arguing that the convergence of recombinant sourcing, smart composite design, and advanced biofabrication is poised to overcome historical limitations and unlock the full potential of collagen for patient-specific regenerative therapies.