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Art Cooking: Henri Toulouse-Lautrec & Osteoclast / Bone Remodeling

The other day I randomly changed the channel to Turner Classic Movies and Moulin Rouge was on. It wasn't the recent remake from Baz Luhrmann. It was one from 1954, which focused on Henri Toulose-Lautrec's life!

Henri Toulouse-Lautrec was an artist and painter in the 19th century who is most famous for his paintings and drawings of the Moulin Rouge. You have probably seen replicas of his large paintings and prints in restaurants or cafes. He also had a bone disease which is known as Toulouse-Lautrec Syndrome or Pycnodysostosis.

Henri de Toulouse-Lautrec, Art Institute of chicago


"A mutation of the gene that codes the enzyme cathepsin K (CTSK) on chromosome 1q21 causes PYCD. Cathepsin K plays a key role in bone remodeling. In particular, it breaks down collagen, a protein that acts as scaffolding to support minerals such as calcium and phosphate in bones. The genetic mutation that causes Toulouse-Lautrec syndrome leads to the buildup of collagen and very dense, but brittle, bones."


When he was young, he would break his bones and have a lot of time to recuperate, which he spent drawing and painting. Interestingly, it's possible that he would not have been a painter if he didn't have the syndrome.

To represent what I learned, this month for #ArtCooking, I decided to do a representation of an osteoclast with less cathepsin K which could happen Pycnodysostosis or they may have normal amount of cathepsin K that is less functional or non-functional (not sure). Anyways, it's just for fun. I chose this graphic when I was looking around because if you didn't know what it was about just by looking at it, it just kind of looks like a snowglobe, which fits with the season and time of year! Haha! :)

"Therapeutic targets in the osteoclast. With the help of av3 integrin, the osteoclasts adhere to the bone surface and form sealing zones. It is produced a highly acidic microenvironment which is essential for the catalytic activity of enzymes such as cathepsin K. Odanacatib inhibits cathepsin K, a lysosomal protease that degrades collagen. Src kinase plays a crucial role in the activity of osteoclasts and it can be inhibited by saracatinib. RANKL acts as essential regulator in the differentiation and activity of osteoclasts. Denosomab, a totally human monoclonal antibody, prevents RANKL from binding to its receptor. FAK: focal adhesion kinase; NF·kB: nuclear factor kappa B; PI3K: phosphatidylinositol 3-kinase; RANK: receptor activator of NF-kB; RANKL: RANK ligand; TRAF-6: tumor necrosis factor receptor associated alpha-6; Src: kinase which regulates cell growth. Adapted and modified from Rachner TD, Khosla D, Hofbauer LC. Osteoporosis: Now and the future. Lancet. 2011;377:1276–87. "

New therapies in osteoporosis

May 2016

DOI: 10.1016/j.rcreue.2016.04.006


Andrés Felipe Posada, Hernán Darío Aguirre, Julio Garcia, Jhon Darío Lodoño Patiño ===

What I used:

- Easy sugar cookies and non-royal icing icing


- Multicolor ssprinkles, Mini M&M, ,chrome sprinkle, gold star sprinkle

- Black gel icing

- Bone (light pink areas) -- Marshamallow fondant


I just free hand drew a snow globe shape.

Here's the finished osteoclast / bone remodeling cookie!

The gold star sprinkles are RANKL and RANK receptor in black gel icing to TRAF-6 and NF-kB. On the left, you can see the PI3 kinase pathway. On the right you can see some lysosome and cathepsin (chrome sprinkles).

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