#osteoclasts

[bpod-bpod]

Breakdown Prevention

Replacing weathered planks on a boat might keep you afloat, but if an over-zealous skivvy starts ripping up planks with abandon, the ship’ll sink before repairs can be made. Osteoclasts are the body’s enthusiastic dismantlers, breaking down bone to enable reinforcements when needed. New research has identified the captain that keeps these vigorous workers in check: a protein called moesin. Individual osteoclasts fuse together via tunnel-like nanotubes (pictured, a bridge stretching between cells) to form large, powerful cells capable of breaking down bone, and moesin regulates this by controlling how tightly the cytoskeleton (the cell's inner protein scaffolding) is attached to the cell membrane. Without it, the team found that cell membranes were more flexible, cells fused together more easily, and created larger zones of contact with bone. Moesin prevents osteoclasts from becoming too big, too fused, and too destructive, maintaining healthy bone balance and perhaps presenting a new therapeutic target in diseases like osteoporosis.

Written by Anthony Lewis

Image from work by Ophélie Dufrançais and colleagues

Institut de Pharmacologie et Biologie Structurale (IPBS), Université de Toulouse, Centre National de la Recherche Scientifique, Université Toulouse III - Paul Sabatier (UT3), Toulouse, France

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in Journal of Cell Biology, October 2025

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[biology-geology-beaches-india]

The Scientific Research Notes of S. Sunkavally, Printed Part, page.195.

Dates unclear, but certainly between 2006-2012.

[fluffykittyscientist]

Osteoclasts are creepy... they are multiple cells fused... imagine a human made by fusing humans and the created human has 50 brains...

[lifeinpoetry]

We don't notice the small fractures in our lives  unless it is too late. Yet the way my father talks it is as though 

no body is afraid of itself. I take comfort in knowing that part of me is made for self-destruction. That it is trying to be better.

— Madeleine Wattenberg, from “Osteoclasts,” published in Sixth Finch

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Monocyte, Microlith, Mineral?

Every breath can be a struggle if you have the rare lung disease pulmonary alveolar microlithiasis. It’s caused by a faulty protein in the membranes of cells that line alveoli, tiny air sacs that fill your lungs. This causes mineral structures called hydroxyapatite microliths to form inside alveoli. Researchers now investigate this process by analysing RNA – a marker for gene activity – in lung tissue from human patients and a mouse model of the disease. Looking at immune cells called monocytes, which can develop into bone-degrading cells called osteoclasts, the team found that osteoclast-related genes were activated in alveolar monocytes. They also found that microliths, pictured using scanning electron microscopy at different resolutions in human (top) and mouse (bottom) lung tissue, contained osteoclast enzymes. This suggests that in response to microliths forming, osteoclast-like cells kickstart into action. This may present a new research avenue for pulmonary alveolar microlithiasis therapies.

Written by Lux Fatimathas

Image adapted from work by Yasuaki Uehara and colleagues

Department of Internal Medicine, Division of Pulmonary, Critical Care, and Sleep Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in Nature Communications, March 2023

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Show Your Teeth

Phagocytes are immune cells with a big appetite. They usually engulf whole pathogens, but this phagocyte has been fooled – placed over a glass plate loaded with tempting antibodies it stretches out over something it can never consume. This ‘frustrated’ phagocytosis allows researchers to peek at the molecular machinery involved, poking a microscope into the opening 'jaw' of a phagocyte. A technique called iPALM highlights its skeleton of tiny actin filaments that rearrange to form rings of pointy structures called podosomes – sometimes known as phagocytic teeth – used to latch onto targets at the beginning of phagocytosis. Rainbow colours highlight actin fibres at different depths, giving researchers hints to the 3D structure of podosomes, that future drug treatments may influence to improve the fight against disease-carrying pathogens.

Written by John Ankers

Image from work by J. Cody Herron, Shiqiong Hu and Takashi Watanabe, and colleagues

University of North Carolina at Chapel Hill, Chapel Hill, NC, USA

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in Nature Communications, July 2022

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Nanoscale Remodelling

Remodelling is complicated, whether it's your house or your bones. Bone remodelling happens when your bones are damaged, whether that's a fracture or everyday strain. Cells called osteoclasts jump into action to break down old bone so new bone can form. Anchoring themselves to the bone, they form a ring-like structure called the sealing zone, into which bone-degrading substances are released without leaking away. Projections made of actin – podosomes – help form the sealing zone, but their organisation at the nanoscale level is unclear. Researchers use super-resolution microscopy to investigate. Human osteoclasts, containing fluorescently tagged actin, were live imaged adhering to bone (pictured). This revealed densely packed actin cores, which form the centre of podosomes, in the sealing zone. Further analysis revealed the activity of these cores was synchronised locally, with groups of cores surrounded by adhesion proteins. This shines a light on the nanoscale lives of podosomes in bone remodelling.

Written by Lux Fatimathas

Video from work by Marion Portes and colleagues

Institut de Pharmacologie et de Biologie Structurale, Université de Toulouse, CNRS, UPS, Toulouse, France

Video originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in eLife, June 2022

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Breaking Bones

Reshaping a bone, like renovating a building, makes a lot of mess. Old cells and debris must be cleared to make space for new, fresh growth. Researchers know that osteoclast cells break down old bone, but what about the spongy cartilage often found where bones meet? This three-week old mouse femur, scanned under a confocal microscope, highlights patterns of blood vessels (red) and cell nuclei (blue), but also elusive cells known as septoclasts (green). They lurk near the growth plate (top) – where cartilage is gradually replaced by hardened bone in early life. Researchers find chemical signals that call septoclasts to action, helping with this ossification. They help during healing too, but as fractures heal slowly in later life, the next challenge is to find ways to boost septoclasts in their vital cartilage clearing.

Written by John Ankers

Image from work by Kishor K. Sivaraj and colleagues

Max Planck Institute for Molecular Biomedicine, Department of Tissue Morphogenesis, and University of Münster, Faculty of Medicine, Münster, Germany

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in Nature Communications, January 2022

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