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Bone and Dental Protein Studies
Research Guide
What is Bone and Dental Protein Studies?
Bone and Dental Protein Studies is a research field examining the roles of proteins such as osteopontin and matricellular proteins in biomineralization, inflammation, immune regulation, cancer progression, cell signaling, dentinogenesis imperfecta, tumor metastasis, and autoimmune demyelinating disease.
The field encompasses 36,741 works focused on proteins that modulate cell function and tissue responses to injury. Studies highlight osteopontin's involvement in biomineralization and dentinogenesis imperfecta alongside matricellular proteins' effects on inflammation and immune regulation. Research also addresses protein influences on cancer progression and tumor metastasis through cell signaling pathways.
Topic Hierarchy
Research Sub-Topics
Osteopontin in Biomineralization
This sub-topic studies osteopontin's role as an mineralization inhibitor in bone and dentin formation via hydroxyapatite binding. Researchers use knockout models and biophysical assays to elucidate crystal nucleation mechanisms.
Osteopontin in Tumor Metastasis
Investigations focus on osteopontin's promotion of cancer cell migration, invasion, and bone metastasis through integrin signaling. Studies correlate plasma levels with prognosis in breast, prostate, and lung cancers.
Matricellular Proteins in Bone Repair
This area examines non-structural proteins like osteopontin and SPARC in modulating osteoblast recruitment and angiogenesis during fracture healing. Research uses transgenic models and scaffolds to study tissue regeneration.
Dental Pulp Stem Cells
Researchers characterize mesenchymal stem cells from human dental pulp for odontogenic and osteogenic differentiation potential. Studies evaluate isolation protocols, immunomodulation, and clinical translation for pulp regeneration.
Osteopontin in Immune Regulation
This sub-topic explores osteopontin's cytokine-like functions in T-cell polarization, macrophage activation, and autoimmune diseases like MS. Functional studies dissect RGD-independent signaling in inflammation.
Why It Matters
Bone and Dental Protein Studies contribute to understanding bone formation mechanisms, as Urist (1965) demonstrated that degradation products of dead bone matrix stimulate histiocytes and inflammatory cells to repopulate implant sites, enabling de novo bone formation by autoinduction with 5522 citations. In dental applications, Gronthos et al. (2000) isolated postnatal human dental pulp stem cells (DPSCs) capable of dentinal repair through odontoblast precursors, forming ectopic dentin and pulp tissue in vivo, cited 4486 times. These findings support tissue engineering scaffolds, with Bose et al. (2012) reviewing advances in scaffolds for bone regeneration, cited 2098 times, and inform treatments for conditions like dentinogenesis imperfecta by elucidating protein roles in mineralization and cell adhesion via RGD sequences as detailed by Ruoslahti and Pierschbacher (1987) with 4863 citations.
Reading Guide
Where to Start
"Bone: Formation by Autoinduction" by Marshall R. Urist (1965) provides a foundational description of bone formation mechanisms through matrix degradation products stimulating cellular repopulation, making it accessible for initial understanding of protein roles in biomineralization.
Key Papers Explained
Urist (1965) "Bone: Formation by Autoinduction" establishes autoinduction via matrix degradation, which Wozney et al. (1988) "Novel Regulators of Bone Formation: Molecular Clones and Activities" builds on by identifying bone morphogenetic proteins (BMPs) as critical extract components directing cartilage and bone formation. Ruoslahti and Pierschbacher (1987) "New Perspectives in Cell Adhesion: RGD and Integrins" connects via cell adhesion molecules containing RGD sequences essential for matrix interactions, while Gronthos et al. (2000) "Postnatal human dental pulp stem cells (DPSCs) in vitro and in vivo" extends to dental proteins by isolating DPSCs for dentinal repair. Komori et al. (1997) "Targeted Disruption of Results in a Complete Lack of Bone Formation owing to Maturational Arrest of Osteoblasts" demonstrates genetic necessities in osteoblast maturation underlying these processes.
Paper Timeline
Most-cited paper highlighted in red. Papers ordered chronologically.
Advanced Directions
Studies emphasize matricellular proteins in modulating cell signaling and tissue injury responses, with top papers focusing on BMPs, DPSCs, and collagen stability. No recent preprints or news in the last 12 months indicate steady incorporation of established findings into related fields like osteoarthritis mechanisms and heterotopic ossification.
Papers at a Glance
| # | Paper | Year | Venue | Citations | Open Access |
|---|---|---|---|---|---|
| 1 | Bone: Formation by Autoinduction | 1965 | Science | 5.5K | ✕ |
| 2 | New Perspectives in Cell Adhesion: RGD and Integrins | 1987 | Science | 4.9K | ✕ |
| 3 | Postnatal human dental pulp stem cells (DPSCs) <i>in vitro</i>... | 2000 | Proceedings of the Nat... | 4.5K | ✕ |
| 4 | Targeted Disruption of Results in a Complete Lack of Bone Form... | 1997 | Cell | 4.2K | ✓ |
| 5 | Novel Regulators of Bone Formation: Molecular Clones and Activ... | 1988 | Science | 3.9K | ✕ |
| 6 | Collagen Structure and Stability | 2009 | Annual Review of Bioch... | 3.6K | ✓ |
| 7 | Self-Assembly and Mineralization of Peptide-Amphiphile Nanofibers | 2001 | Science | 3.6K | ✕ |
| 8 | Picrosirius staining plus polarization microscopy, a specific ... | 1979 | The Histochemical Journal | 2.5K | ✕ |
| 9 | Recent advances in bone tissue engineering scaffolds | 2012 | Trends in biotechnology | 2.1K | ✓ |
| 10 | Stem Cell Properties of Human Dental Pulp Stem Cells | 2002 | Journal of Dental Rese... | 2.1K | ✕ |
Frequently Asked Questions
What role do dental pulp stem cells play in dentinal repair?
Postnatal human dental pulp stem cells (DPSCs) isolated from pulp tissue act as precursors to odontoblasts responsible for dentinal repair. Gronthos et al. (2000) showed these clonogenic, proliferative cells form ectopic dentin and associated pulp tissue in vivo. Stromal-like cells from DPSCs reestablish in culture after transplantation.
How does bone formation occur by autoinduction?
Bone formation by autoinduction involves degradation products of dead bone matrix stimulating wandering histiocytes, foreign body giant cells, and inflammatory connective-tissue cells to repopulate implant sites. Urist (1965) observed histiocytes as the most numerous cells transferring collagenolytic activity. This process initiates cartilage formation leading to de novo bone.
What is the function of RGD in cell adhesion proteins?
The tripeptide arginine-glycine-aspartic acid (RGD) serves as the cell recognition site in many adhesive proteins in extracellular matrices and blood. Ruoslahti and Pierschbacher (1987) identified RGD in proteins facilitating molecular interactions for cell adhesion. These interactions involve integrins in bone and dental protein contexts.
What happens in the targeted disruption of the gene resulting in lack of bone formation?
Targeted disruption of the gene leads to complete lack of bone formation due to maturational arrest of osteoblasts. Komori et al. (1997) demonstrated this effect through disrupted osteoblast development. The study highlights the gene's essential role in bone formation processes.
How do peptide-amphiphiles contribute to mineralization?
Peptide-amphiphiles self-assemble via pH induction into nanofibers mimicking extracellular matrix for mineralization. Hartgerink et al. (2001) showed reversible cross-linking enhances nanofiber integrity post-mineralization. These scaffolds support biomineralization relevant to bone and dental tissues.
What defines the structure of collagen in bone and dental studies?
Collagen forms a right-handed triple helix bundle of three parallel left-handed polyproline II-type helices as the most abundant animal protein. Shoulders and Raines (2009) detailed the physicochemical basis for its stability. This structure underpins biomineralization and tissue integrity.
Open Research Questions
- ? How do matricellular proteins like osteopontin precisely regulate immune responses in autoimmune demyelinating diseases?
- ? What molecular pathways link osteopontin to tumor metastasis in bone and dental tissues?
- ? How can dental pulp stem cell differentiation be optimized for dentinogenesis imperfecta treatments?
- ? What are the exact mechanisms by which RGD-integrin interactions influence biomineralization rates?
- ? How do degradation products of bone matrix interact with histiocytes to control inflammation in injury repair?
Recent Trends
The field maintains 36,741 works with no specified 5-year growth rate.
Top-cited papers from 1965 to 2012 dominate, including Urist at 5522 citations and Gronthos et al. (2000) at 4486 citations, reflecting sustained interest in bone autoinduction and dental stem cells.
1965Absence of recent preprints or news coverage in the last 12 months points to integration into broader topics like systemic lupus erythematosus research and musculoskeletal synovial treatments.
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