Staphylococcus aureus bacteria invading a bone cell via fibronectin bridges.

Unlocking the Secrets of Staphylococcus Aureus: How Bacteria Invade Your Bones

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Rhea Morgan in Health & Wellness November 2025 • 4 min read.

"Decoding the process of Staphylococcus aureus internalization by osteoblasts, and what it means for treating bone infections."


Staphylococcus aureus is a common bacterium, often found on the skin or in the nose, and is a leading cause of implant-related orthopedic infections. While it was once believed to primarily exist outside of cells, research has revealed its ability to invade eukaryotic cells, including those in bone tissue. This discovery has transformed our understanding of how these infections take hold and persist.

The initial step in Staphylococcus aureus infection is adhesion to the tissues surrounding an implant. This adhesion sets the stage for the bacteria to internalize, or enter, the host cells. Once inside, the bacteria can evade the body's natural defenses and antibiotic treatments, leading to chronic and difficult-to-treat infections like osteomyelitis.

Recent studies have focused on the specific mechanisms that Staphylococcus aureus uses to invade bone cells, particularly osteoblasts, which are responsible for bone formation. By understanding these processes, scientists hope to develop more effective strategies to prevent and treat implant-related infections.

The Role of Adhesins and Fibronectin in Bacterial Internalization

Staphylococcus aureus bacteria invading a bone cell via fibronectin bridges.

Adhesins, also known as MSCRAMMs (Microbial Surface Components Recognizing Adhesive Matrix Molecules), are essential for Staphylococcus aureus to interact with bone matrix proteins such as fibronectin, collagen, and bone sialoprotein. These interactions facilitate the bacteria's attachment to bone tissue, allowing them to colonize the area and initiate the infection process.

Fibronectin, a protein found in the extracellular matrix of bone, plays a crucial role in the internalization of Staphylococcus aureus. The bacteria use fibronectin-binding proteins (FnBPs) to attach to fibronectin, which then acts as a bridge to connect the bacteria to the osteoblasts. This interaction triggers the internalization process, allowing the bacteria to enter the bone cells.

  • FnBPA: Appears to play a crucial role in the internalization process.
  • CNA and Bbp Adhesins: Can play a synergistic role by acting in the initial adhesion of S. aureus to osteoblasts, thus favoring the subsequent FnBPA-mediated internalization.
  • Genetically Different Strains: Different strains of S. aureus exhibit varying abilities to adhere and internalize due to differences in their genetic makeup, particularly in the genes coding for adhesins.
Researchers have been studying different strains of Staphylococcus aureus to understand how variations in their genetic makeup affect their ability to adhere to and invade osteoblasts. By comparing strains with different adhesin profiles, they can pinpoint the specific adhesins that are most important for the infection process and the internalization process. These studies often involve in vitro models using osteoblast cell lines to mimic the conditions within bone tissue. For example, MG63 osteoblasts are frequently used as the eukaryotic cells tested for internalization ability.

Future Directions and Therapeutic Implications

Understanding the mechanisms by which Staphylococcus aureus adheres to and invades bone cells opens the door to new therapeutic strategies. By targeting specific adhesins or the fibronectin-mediated internalization process, researchers hope to develop treatments that can prevent or disrupt bone infections. This may involve designing drugs that block the interaction between bacterial adhesins and bone matrix proteins or developing vaccines that stimulate the immune system to target these bacteria more effectively. Continued research in this area is essential for improving the outcomes of patients with implant-related orthopedic infections and osteomyelitis.

About this Article -

This article was crafted using a human-AI hybrid and collaborative approach. AI assisted our team with initial drafting, research insights, identifying key questions, and image generation. Our human editors guided topic selection, defined the angle, structured the content, ensured factual accuracy and relevance, refined the tone, and conducted thorough editing to deliver helpful, high-quality information.See our About page for more information.

Everything You Need To Know

1

How does Staphylococcus aureus initially attach to bone tissue to begin an infection?

Staphylococcus aureus uses adhesins, specifically MSCRAMMs (Microbial Surface Components Recognizing Adhesive Matrix Molecules), to attach to bone matrix proteins like fibronectin, collagen, and bone sialoprotein. This attachment is essential for the bacteria to colonize bone tissue and initiate infection. Without these adhesins, Staphylococcus aureus would struggle to establish a foothold, making them a prime target for therapeutic intervention.

2

What role does fibronectin play in the internalization of Staphylococcus aureus into bone cells?

Fibronectin, found in the extracellular matrix of bone, is critical for Staphylococcus aureus internalization. The bacteria uses fibronectin-binding proteins (FnBPs) to latch onto fibronectin, which then acts as a bridge connecting the bacteria to osteoblasts, triggering internalization. Without fibronectin, Staphylococcus aureus's ability to invade bone cells would be significantly hampered, making it a key target in preventing chronic bone infections.

3

How do different adhesins like CNA and Bbp contribute to the internalization process of Staphylococcus aureus?

The initial adhesion of Staphylococcus aureus to osteoblasts is often facilitated by adhesins like CNA and Bbp, which work synergistically with FnBPA to enhance internalization. While FnBPA plays a crucial role in internalization, CNA and Bbp aid in the initial attachment, setting the stage for FnBPA-mediated entry into the bone cells. Without this synergistic action, the efficiency of Staphylococcus aureus internalization could be reduced.

4

Why do different strains of Staphylococcus aureus exhibit varying abilities to infect bone?

Different strains of Staphylococcus aureus exhibit varying abilities to adhere and internalize due to genetic differences, particularly in the genes coding for adhesins. These variations affect the bacteria's capacity to colonize and infect bone tissue, influencing the severity and persistence of infections. Understanding these genetic differences can help in developing targeted treatments specific to different Staphylococcus aureus strains.

5

What are the potential future therapeutic strategies for treating bone infections caused by Staphylococcus aureus, based on understanding its invasion mechanisms?

Targeting specific adhesins or the fibronectin-mediated internalization process in Staphylococcus aureus offers promising therapeutic strategies for preventing or disrupting bone infections. This approach involves designing drugs that block the interaction between bacterial adhesins and bone matrix proteins or developing vaccines to stimulate the immune system to target these bacteria more effectively. Such targeted interventions could significantly improve outcomes for patients with implant-related orthopedic infections and osteomyelitis.

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