I have been slow about posting blogs due to the recent conferences attendance. I will talk about them in the post to come; there was great cutting-edge science presented at both AHA Sessions as well as Kidney Week. I also decided to share this experience because it is my life for the next several weeks. Let me know what you think about this writing style since it is a bit different. With that being said, let’s get to it.
If you all are following me on twitter (I hope you are), you know I was in Anaheim, CA working a scientific minority meeting. Upon returning I decided to prepare for the holiday. If you are anything like me, I have a ‘honey do’ list a mile long. Well, top priority was to finish tiling the shower and painting the bathroom ceiling. Being the “do it yourselfer” that I am, I went to the store, got the supplies, and went to work. I successfully installed all the tile and started grouting, when I fell!!! That unfortunate accident resulted in my arm being broken in several places including the radius and ulna. I am fine and healing well, but I’d like to share some roadblocks that come along with having a broken bone and lupus (SLE; systemic lupus erythematosus).
First, SLE is an autoimmune disease whereby the immune system attacks its own body resulting in widespread inflammation and tissue damage. The most common symptom is the butterfly pattern rash across the bridge of the nose. However, other symptoms include stiffness, lack of energy, hair fall, and cardiovascular disease (CVD). I was diagnosed years ago, hence in a previous blog, I discussed how a sever flareup caused me to come out of denial to respect the consequences of the disease. That was literally a life changing experience. One noteworthy symptom of SLE is avascular necrosis (AVN), also known as osteonecrosis; which leads me to the point of this blog. AVN is characterized by reduced blood flow and increased pressure around parts of a bone making it difficult for bone formation (ossification) to occur. AVN can be a result of trauma, SLE, as well as CVD; namely, hypertension, renal disease, diabetes, vasculitis or arthritis. However, despite these clinical variables, a person can be genetically predisposed, have metabolic factors, or abnormal blood supply and shape that could contribute to the pathophysiology (onset) of AVN. For me, having both SLE and CVD I was concerned about my healing process. Especially after going to the doctor, having my cast removed, and no significant healing in my fractured areas. I had more questions than answers after the orthopedic visit so, as any curious person, I took to the research and clinical acquaintances to find answers. That led to more questions by the way.
It is well known that SLE is characterized by autoantibody formation with intermittent inflammatory periods (flare ups). What I found was that the type of collagen (I, II, or III), fibrinogen, fibronectin, actin, and MSE55 distribution contributed to the rate at which bones healed. SLE modulated this attraction, distribution and formation if these components. Since MSE55 was robustly found in nonhealing fractures and I had never heard of MSE55, I started reading more about its impact on nonhealing fractures, hehehe. According to Dominiak et al 2018, MSE55 can potentially lead to bone defects and nonhealing due to its pivotal role in actin polymerization. Using immunostaining, this group was able to determine MSE55 colocalized in the endothelial cells and the cellular process of osteocytes (bone cells). A mutation in the protein complex hindered proper cell formation resulting in slow to nonhealing.
Regarding collagen, it was suggested the collagen type II (normally dominant form) was deceased, irregular, and in some cases absent, in patients with SLE. Oddly, collagen type III was significantly increased in fibrotic foci near trabeculae, cyst wall, and blood vessel walls; while collagen type I was reduced or absent in SLE samples all together. Indeed these data suggested an increase in immunoglobins (IgG & IgM), mononuclear cells (lymphocytes and monocytes; cells used in defense of immune reaction), and complement were indicative of an immune response that could hamper the healing process.
With all that has been said, what are your thoughts? Do you think going to an orthopedic specialist is enough in a person with SLE or do you think the Rheumatologist should be involved? With these changes in collagen patterns, would you imagine a person could benefit from collagen loading to assist in the healing process?
This is a lot of information, but let’s discuss these options in more detail so we can learn together. With increasing numbers of breaks and fragility among the elderly we should know more. Post your thoughts or questions in the comments. Follow me on social media where I post updates daily; I am @AnberithaT on all platforms (Facebook, Twitter, & Instagram). I look forward to getting healthy together.
- J Rheumatol 2018; 45:1462-1476
- Ultrastructural Pathology 2005; 29:107-120