Category: Knee injury

6 tips for weeding your mental garden
I love gardening, tilling the soil, planting little seeds and watching them grow. A few weeks ago, while picking crabgrass from the kale, I found myself thinking about my clients and their concerns about bone health. I was thrilled to think about the extent to which mental and emotional stress robs us of both happiness and bone health. With this thought in mind, a “Garden life” metaphor came to mind. The metaphor was simple and applies to backyards as well as mental landscapes. The metaphor is: “Nourish the desired and remove the unwanted.”

Two weeks later, after attending the revival of Acharya Shunya Roar like a goddess workshop, I was inspired to write this one 6 tips for weeding your mental garden. They are simple “Acharya Shunya-inspired” self-awareness exercises that you and I can use to create inner peace and a mind that works for us, not against us. (In case you haven’t heard of her work, Acharya Shunya is a leading spiritual leader of our time, a best-selling author, a Vedic scholar, and the first female custodian of a 2,000-year-old Vedic wisdom lineage. I had the great fortune to recently interviewed her at the Omega Institute. At the end of this blog, you can learn more about her work and how to enjoy this wise video interview.)

This is how the story goes and here are your 6 powerful tips for creating the bone strength and destiny you desire:

Every spring, six of my friends and I plant a beautiful vegetable garden in the backyard. While none of us are expert gardeners, we enjoy watching the bloom of life and thinking of ways to nourish this new life with fertilizer, water, sunshine and our love. We also keep an eye on weeds as unwanted visitors can easily take over the entire garden if not kept in line. The more we care for our garden, the more beautiful and fruitful it becomes.

The garden-life metaphor

What I realized was that we plant “seeds” in our minds with every thought, belief, desire, and intention. These ‘seeds’ can be life-sustaining positive thoughts that carry an energy of appreciation, happiness, contentment or even love. Or the thought may carry an energy of negativity, blame, anger, worry and even fear. In our mindscape we fertilize these ‘thought seeds’ by the attention we pay to them. Whether we are aware of it or not, what we focus on becomes more powerful in our daily lives and in our mental garden.

Just as we can produce a richer and more beautiful garden if we limit the weeds, we can with awareness control the unwanted “mental weeds” that take up space and spread their vibration throughout our entire mindscape.

And what exactly are ‘mental weeds’?

“Mental weeds” are repetitive thoughts and beliefs that invade and disrupt the natural, calm, peaceful, and happy feelings in our minds. These weeds are disruptive, negative, voluntary mental pop-ups that include fear, self-doubt, anger, worry and anxiety. The mental and emotional negativity of this “thought weed” has been well documented as a contributing factor to many chronic degenerative diseases, including osteoporosis (as described in the Better Bot Solutions Course and my blog, How bot responds to danger).

This mind-body connection is well established. The Bible says that, for example “A cheerful heart is good medicine, but a crushed spirit dries up the spirit bones.(Proverbs 17:22) Even more striking is the 5,000 year old Ayurvedic wisdom that Acharya shared with me. She said that in our conversation another word for ‘health’ in the ancient Vedic texts was ‘happiness’. The crowning achievement of all this came at the end of our interview, when Acharya Shunya applauded me for discovering that worry and fear damage the bone. She talked about the fact that ancient Vedic texts mention this Bone is the strongest material in the body, the strongest, but the only thing that can erode it is negativity. Thinking about those pearls of wisdom fueled my motivation to increase the level of my mental/emotional gardening!

6 tips for weeding your mental garden

Inspired by the Vedic scholar Acharya Shunya
1. Take inventory of your thoughts.
- Experiment with focusing on one thought and recording the “feel” of the thought. Was the thought associated with a feeling of well-being or even contentment? Or was it critical of others or yourself? Was it humiliating to yourself or to someone else? Was it a good feeling?
- Ask yourself, “Is this a thought or belief that I want to continue and influence in my life every day?” Or can I just let this article pass?
- Be aware and remind yourself that the thoughts you repeat over and over become the strongest weeds.
1. Do some mental housekeeping.
- Remember: you are not your thoughts. You are the witness of your mental wanderings.
- With practice you can create a little distance between yourself and your thoughts.
- You can become a witness to your thoughts. You can realize yourself as the consciousness behind your thoughts.
- As a witness, you then consciously choose which thoughts you want to strengthen and which thoughts you want to let through.
- Once again, remember that what you focus your attention on will become stronger in your life.
- Remove the thoughts and associated feelings that you would rather not have in your life.
- Moreover, you don’t have to hold on to every thought; you have enough left.
- In fact, you have about 90,000 thoughts a day, most of which passed through your mindscape yesterday.
- As spiritual teacher Eckhart Tolle suggests, it’s a good habit not to take your thoughts so seriously.
1. Meditate on the wisdom of this ancient Vedic observation that Acharya taught me:
- Every action leads to habit.
- Every habit builds character.
- And character leads to fate.
- As she suggests, don’t give space in your beautiful mind to a single thought without purpose.
1. Make your mind your servant, not your master.
- When your mind is in turmoil or overshadowed by worries, stop whatever you are doing.
- Take a few deep breaths and shift your attention to what it feels like to breathe in and out.
- Creating even a small space between you and your worrying thought calms the mind.
- Then ask yourself, “Can I acknowledge this thought and the associated feeling and then let it go?”
- Or should I do a reality check to verify whether what I think is actually true?
- Or is it time to gather my sovereign power and address the situation?
1. Be kind and gentle to yourself and others.
- Remember that it is the nature of the mind to move quickly, just as it is the nature of the monkey to jump from branch to branch.
- You can’t always control your monkey mind.
- However, your sovereign self can witness the thoughts, and you realize that you are not your mind.
- You can create a gap between your thoughts and emotions and your deepest self.
- As you repeatedly rest in this gap, gently sow the seeds of your desires and imagine the mental landscape you desire.
1. Check your mental/emotional tone every morning when you get up.
- Where did your thoughts wander during the night, what are your feelings?
- When I wake up cheerful and happy, I am grateful to the great goddess for a refreshing sleep.
- If I wake up less cheerful, I immediately call on one of my inspiring spiritual teachers, consciously setting a higher vibration.
- You might start by asking yourself: What vibrational tone do I want for today?
- Consciously determine the tone you want to spend the day.
- And then ask: what can I do to move my energy field in that direction?
- There are countless activities that are cutting edge, and the choice is yours. Options include meditation, prayer, reading or listening to uplifting speakers, wisdom teachings or scriptures, taking a sunrise walk, hitting the yoga mat, music, chanting. The tone options are endless. Enjoy it and see what works best for you.
In closing, let me say that this is easier than you might think. As Acharya reminded me, it takes some time to change the constitution/organization of the physical body; you don’t change the bone fragility score overnight. But the constitution/organization of the mind can change in a flash. If you change your mind, you immediately change your life!

So let’s all get started! Do the work, start designing a mind that serves your bones and your greatness! I’ll be there next to you.

Join my upcoming video interview with Acharya Shunya on YouTube on October 5 by clicking Notify Me on my YouTube channel

Acharya Shunya’s website: awakensself.com

The books of Acharya Shunya:
- Ayurveda lifestyle wisdom: A complete recipe to optimize your health, prevent diseases and live with vitality and joy, Sounds true, 2017.
- Sovereign self: Claim your inner joy and freedom with the empowering wisdom of the Vedas, Upanishads and Bhagavad Gita, Sounds true, 2020.
- Shout like a goddess: Every woman’s guide to becoming unapologetically powerful, prosperous and peaceful, Sounds true, 2022.
I am Dr. Susan E. Brown. I am a clinical nutritionist, medical anthropologist, writer and motivational coach speaker. Learn my proven 6-step natural approach to bone health in my online courses.
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October 18, 2023
How Sleep Improves Bone Health – Bone Talk
You’ve probably heard someone say that children seem to grow bigger overnight evidence gathered from extensive research suggests that this is probably true. Many people have a busy schedule that prevents them from sleeping well. However, you should not forget that good sleep is good for your mental state And physical health. This is how sleep affects your bone health.

The Healing Power of Zzz’s: Sleep and Bone Remodeling

Your body constantly renews, repairs and grows its bones. There is a direct correlation between the amount of sleep you get and the health of your bones. Researchers have made the link individuals who receive shorter sleep duration have lower bone mineral density and a higher risk of osteoporosis. The study, conducted in postmenopausal women, found that women who get five or fewer hours of sleep per night have lower bone mineral density in the spine, neck, hip and even across the body.

Several healthy processes are affected by the amount of sleep you get, and one of these processes is bone remodeling. Your body’s special bone cells, osteocytes, manage bone remodeling. These cells cause various actions in the body, such as helping your bones maintain optimal mineral levels and healing damaged areas. For example, the cells will activate other cells known as osteoclasts, causing them to remove minerals from your bones if your calcium levels get too low. The cells also give rise to osteoblasts, which help them rebuild and repair your bones if you suffer several fractures. The bone remodeling processes are likely to be less effective for individuals who do not get enough rest.

Level up: Improve your sleep hygiene for better bone health

The general rule of thumb is that individuals who sleep and rest longer tend to have healthier bones than those who don’t. Bone growth and repair are facilitated by a good night’s sleep, as the rest gives your body enough time to repair and reshape itself.

Signs of poor sleep hygiene include having trouble sleeping, experiencing daytime sleepiness, and experiencing sleep disturbances. These are the most telling signals; However, another concern to consider is persistently poor sleep quality. Over time, poor sleep hygiene can cause these problems to persist and potentially worsen other health problems.

Creating one healthy sleep routine is important for both your physical and mental health. It improves your productivity and quality. Good sleep hygiene is vital for children and adults; however, it is even more important for individuals likely to be affected by bone-related conditions.

Good sleep habits are good for your health because they create consistency and positive reinforcement for all aspects of life. Good sleep hygiene can be the result of adapting your environment to your needs and establishing the right routines.

Pillow Talk: tips for bone-strengthening sleep

There are many of them steps you can take to improve your sleep experience. You need to optimize your sleep schedule, daily routines, and bedtime routines to help you get better sleep quality. Eat rightget enough fysical activityand create a pleasant environment in which you can relax and fall asleep easily. Here are a few more tips to help you improve your sleep routine:
- Prioritize your sleep: You need to prioritize sleep if you want healthy bones, body and mind. Calculate your ideal sleep duration by taking into account the time you wake up and make this a regular part of your daily routine.
- Set a fixed alarm time: Keeping a consistent wake-up time, regardless of the day of the week, can help you regulate your sleep patterns and improve sleep quality.
- Maintain a regular sleep schedule: Consistency helps synchronize your body’s internal clock.
- Create a sleep-conducive environment: Keep your bedroom dark, quiet and cool. The ideal temperature is about 65-68 degrees.
- Limit screen time before bed: Exposure to blue light from screens can disrupt melatonin production.
- Make gradual adjustments: Try to adjust your sleep pattern gradually. Make adjustments of half an hour or an hour each day until you adjust to your schedule.
- Don’t take many naps: Avoid taking many naps during the day as this can affect your sleep patterns. Keep naps short and limit them to the early afternoon.
- Prioritize nutrition: Avoid heavy meals and caffeine right before bed, opting for sleep-supporting snacks instead.
- Add physical activity: Regular exercise can improve sleep quality, but avoid vigorous exercise before bed.
- Deal with stress: Techniques such as meditation and deep breathing can alleviate sleep-disrupting stressors.
Incorporating these practical tips into your daily life can make a significant difference in both the quality of your sleep and the health of your bones. By taking proactive steps to improve your sleep habits, you’re investing in a healthier, more resilient future for your bones. So go ahead, prioritize sleep and let your body do its nightly magic for stronger, healthier bones. Good night!
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October 18, 2023
Cerapedics Reinforces Commitment to Level 1 Evidence with Long-Term Results from Six-Year Central IDE Cervix Study Showing 98.6% of Spinal Fusions Occurring in Patients Treated with i-FACTOR®

WESTMINSTER, Colo., Oct. 17, 2023 /PRNewswire/ — Cerapedics Inc., a commercial-stage orthopedic company committed to redefining the standard of care for bone repair, today announced long-term follow-up data from its pivotal IDE study of i-FACTOR Peptide-Enhanced Bone Graft. Published data demonstrated single-level anterior cervical discectomy and fusion (ACDF) fusion rates of 98.6% after six years in patients treated with i-FACTOR and reinforce Cerapedics’ commitment to accumulating long-term clinical evidence. In particular, the results support the safety and efficacy profile of i-FACTOR at one and two years, as published in Spine And Neurosurgery.

i-FACTOR has demonstrated statistical superiority over local autograft in overall success* at one- and two-year endpoints for single-level ACDF. i-FACTOR further demonstrated spine fusion rates of 89.7%, 97.3% and 98.6% at one, two and six years, respectively, versus 85.8%, 95.8% and 97.3% for local autograft, with results published in Spine And Neurosurgery. 220 of the original 319 patients were observed for six years or 72 months.

The six-year results, published earlier this year in Neurosurgery, were based on a single-blinded, randomized, controlled prospective study of i-FACTOR compared to local autograft in single-level ACDF, which enrolled a total of 220 patients, including 106 in the i-FACTOR group and 114 in the local autograft control arm. Of the 22 locations from the original IO study, 17 participated in this six-year post-approval study.

“Physicians are looking for long-term safety and efficacy data to support decision-making about the safest and most effective spine technologies,” said Professor Paul Arnold, CARLE Illinois College of Medicine, principal investigator and author of the 12-, 24- and publications from 72 months. “In this unique long-term follow-up data from a pivotal IDE study, i-FACTOR met all four FDA-mandated non-inferiority success criteria and demonstrated safety and efficacy in single-level anterior cervical discectomy and fusion compared to autograft at 12 years of age age. , 24 and 72 months.”

“These results clearly demonstrate the efficacy rates and safety profile of i-FACTOR over time and also reflect Cerapedics’ commitment to producing the highest quality evidence on the use of our products,” said Valeska Schroeder, Chief Executive Officer of Cerapedics. “Combined with the results of the IDE study, these data contribute to the clinical understanding of the efficacy and safety of i-FACTOR. While there are numerous other bone grafting options, many have not undergone the same level of testing. This data has a significant impact on insurance payers looking for Level 1 evidence when making coverage decisions.”

i-FACTOR is available in the US through pre-market approval. It is the most stringent type of marketing application required by the FDA and involves the process of scientific and regulatory review to evaluate the safety and effectiveness of Class III medical devices based on Level 1 clinical trials. Cerapedics is currently conducting its second clinical randomized controlled trial for an indication for transforaminal lumbar interbody fusion (TLIF) involving 290 subjects, which is registered onclinicaltrials.gov.

About i-FACTOR Peptide-enhanced bone graft
i-FACTOR is a Class III FDA-approved bone graft supported by rigorous Level 1 human clinical data from an IDE study published in Spine And Neurosurgery. It is the only spinal bone graft powered by P-15 osteogenic cell-binding peptide, with a precise bone-building mechanism.** i-FACTOR has a demonstrated safety profile and is as safe as local autograft in single-level ACDF with proven statistical superiority overall success* after one and two years.

i-FACTOR Peptide Enhanced Bone Graft is indicated for use in skeletally mature patients for the reconstruction of a degenerated cervical intervertebral disc at one level from C3-C4 to C6-C7. i-FACTOR Peptide Enhanced Bone Graft should be used in an allograft bone ring and with additional anterior plate fixation. For more information, full description of the indication for use, contraindications, safety warnings etc. about i-FACTOR, please visit our website: https://www.cerapedics.com/sites/default/files/2023-08/40002 – 07-4%20Putty%20USA.pdf

About Cerapedia
Cerapedics is a global commercial-stage orthopedic company that aims to redefine the standard of care for bone repair by healing bones faster and faster, without compromising safety, so patients can live their healthiest lives. Bone grafts, including Cerapedics products, are used in more than four million spine, orthopedics, trauma and interventional procedures worldwide each year. i-FACTOR is a Class III FDA-approved product indicated for single-level ACDF. Cerapedics’ new “P-15 Bone Graft” product is currently being evaluated for use in lumbar interbody fusion through ASPIRE, a pivotal clinical trial, and has received Breakthrough Device Designation from the FDA. Cerapedics is headquartered in Westminster, CO.

For more information, please visit us at www.cerapedics.com.

Media contact:
Ten Bridge communications
TBCCerapedics@tenbridgecommunications.com

*Defined as meeting the Fusion, Function (Neck Disability Index), Neurological, and Safety endpoints
**Surface-based mode of action

SOURCE Cerapedics Inc.

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October 18, 2023
Irma Jennings’ Bone Health Test Results (DXA) 2020
DXA 2022
My latest DXA and TBS report has arrived. As a reminder, in 2005 I was diagnosed with osteopenia and given a script for Fosamax. I refused. I was in my fifties. Now I’m in my seventies. My intention was to implement my 7 pillars of bone health for better results:
1. Calcium and mineral rich foods
2. Supplements (Cal Citrate, Vit. D., Vit K2 – Mk7, Dr. McCormick’s Collagen and Mineral Whey)
3. Bioidentical hormones
4. Weight-bearing exercise
5. Stress reduction
6. Sleep hygiene
7. Brings joy to my daily life
At that time, Fosamax was a long-term drug. I would have been a long-term user. I am grateful for the work of Dr. Schneider and who has revealed her terrible story below. Because of her work, Fosamax users are now taking a drug holiday.

The story of Dr. Jennifer Schneider

Dr. Jennifer Schneider was standing on a subway in New York City when the train jolted and Schneider felt a kink in her right leg. It was her femur, the strongest bone in the body.

“I shifted to the right to keep my balance and felt a large crack. I felt it in my thigh. There was no doubt that I had broken my femur,” says Schneider, a semi-retired internist from Tucson, whose The fracture was in the upper third of her thigh.

“It’s extremely unusual to break that part of the femur,” she said. “It just doesn’t happen that way.”

Schneider’s femur fracture occurred in October 2001, but it wasn’t until 2005 that she began to suspect the cause of the strange injury: long-term use of the drug Fosamax, which ironically is prescribed to treat and prevent the bone-thinning disease osteoporosis.

Schneider had been taking the drug since 1995, when she was diagnosed with osteopenia, a condition considered by many doctors to be a precursor to osteoporosis.

“The drug suppresses bone loss and in some people, who knows, it may be doing its job too well. It suppresses too much,” Schneider said.

Fosamax drugs from New Jersey-based Merck say there is no evidence of a link between the drug and femur fractures. But in the interest of patient safety, Merck says it voluntarily amended the Fosamax label in July 2009 to include “low-energy femoral shaft and subtrochanteric fractures” in the side effects section of the label. [1]

IMPORTANT:

In June 2023 I will open my:

Pilot program: Strong Bones – Healthy You
A comprehensive bone health program – the whole body approach.

Click HERE to schedule a free 30 minute session.

This conversation will determine if my program is right for you.

DXA from IRMA

My ninety-minute pilgrimage to the University of Pennsylvania hospital yielded an excellent DXA.

Below are my results

Great results for my hips and spine – everything is moving in the right direction over time.

Not so much my forearm.

Note the colors in the report. We are looking for green.

VEGETABLE

The color chart below will help you understand the ranges.

T-score less than -1 = Normal | COLOR GREEN

T-score between -1 to -2.5 = osteopenia | COLOR YELLOW

T-score greater than -2.5 = Osteoporosis | COLOR RED

TBS L1-L4 = 1.393 (normal is 1.35 and higher)

Below you will find the Trabecular Bone Score or TBS report of my spine. Simply put, the TBS measures the inner bones, while DXA measures the outer bones. Color falls into the vegetable normal area. My inner bones look good.

DXA spine – Normal range L1-L4 = T-score 0.0

Below is my DXA for my spine. It also falls into the vegetable (normal) part.

Measurement of the spine at DXA 2022

DXA hip –

Femoral neck -1.8 Total left hip -1.1

YELLOW – Osteopenia

Also measures in the normal yellow range. Note the DOT in the yellow section.

Forearm

RED – Osteoporosis

Radius 33% = -2.7

Radius 33% is the size used for the forearm.

Irma’s tracking schedule

Click on the image for a better view.

For my readers who like to track their DXA, below is my tracking chart. The diagram shows the type of machine used. Each machine has a serial number. When looking at a DXA comparison, it is essential to know the DXA machine and its serial number. That serial number can usually be found in the lower right corner of your DXA report. All my tests were on GE Lunar Prodigy with the same serial number.

How to get a good DXA

Hips

The legs are turned inward, allowing a good DXA measurement.

Spine

The box places my back flat on the table

Forearm

Next steps

My annual CMP (Comprehensive Metabolic Panel) blood test next year. This test measures the calcium levels that I monitor.

Dr. McCormick uses blood tests to delve deeper into bone health.

Also, my friend, Dr. Lani Simpson, DC, CCD, who has been in the osteoporosis trenches for decades, before I would get and follow bone markers:
- CTX (full name Carboxyterminal cross-linking telopeptide or bone collagen) is a bone resorption marker.
- My CTx was:
- 346 (27-10-22 – Lab Corp)
- 304 (2/22/22) Quest Labs (within the range offered in my Bone Marker presentation
- P1NP (full name Procollagen type 1 N propeptide) measures bone formation. If my doctor does not write a script for this test, I will receive the script through Evexia or Life Extension.
- My previous P1NP was 34
- Vitamin D: I test twice a year – after summer and after winter
- My last test showed 44.9 ng/ml
Dr. Lani Simpson suggested an x-ray of my spine because arthritis makes a DXA look better than it is. My x-ray was taken by Dr. Kim Zambito, who reported mild arthritis in my spine and wrist.

It takes a community.

Forearm

Why is the non-dominant forearm added to the DXA/TBS report?

The spine and hip may have arthritis, but the DXA shows stronger results. The forearm can be a possible indication of problems with the parathyroid gland.

Your forearm consists of 80 to 100% cortical bone. When a person has hyperparathyroidism, too much parathyroid hormone is pumped out. What does that degrade?

That degrades cortical bone more than trabecular bone. And that’s why when you look at someone with hyperparathyroidism, their forearms often have low bone density.
- “Primary hyperparathyroidism: Although this is a systemic disease that affects the entire skeleton, the lowest BMD is often the forearm, which may be the only site where the BMD is less than -2.5. In this case, the result should influence the decision regarding the surgical treatment of primary hyperparathyroidism (PHPT).” [i]
Tests show negative for hyperparathyroidism. Bones are complicated.

We are all different

Several members of my Bones Tribe are on medication because it was deemed necessary based on a complete and comprehensive intake and blood work reviewed by their bone doctor. My Bones Tribe members seek other opinions before making a decision about medication based on knowledge versus fear of a decision.

TIPS

My DXA/TBS score was run on:

The Hospital of the University of Pennsylvania

3400 Civic Center Blvd. – Ground floor

Philadelphia, PA

phone: 215-662-3000 to book a DXA (ask for radiology to book your DXA).

My script reads:
- DXA bone density, axial CPT 77080
- DXA bone density/peripheral CPT: 77081
- Includes TBS and peripheral forearm.
I asked for one full colored copy of my reports Before I left.

I have a good feeling about the results.

MEMORY:

I open my:

Pilot program: Stronger bones – Healthy you

My 8-week Comprehensive Bone Health Program – The Whole Body Approach promises to educate you on every aspect of bone health. From DXA/TBS, bone markers, blood tests, calcium rich foods, exercise. You gain knowledge, a deep understanding of the terminology and move on to empowerment.

Click HERE for a free 30 minute consultation to confirm that my program is right for you.

I hope my shared experience is helpful to you and your beautiful bones.

From my loving bones to yours,

Irma Jennings, INHC, holistic bone coach

e-mail: [email protected]

[1] https://www.drug-injury.com/drug_injury/2010/09/doctor-files-suit-says-bone-drug-leads-to-breaks.html

Let me support your bones

Receive an in-depth, tailor-made private session

Book a private coaching with Irma now

Join our amazing Bone Tribe community

Get the support and information you need to live fearlessly with your bone diagnosis
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October 18, 2023
What does my KOOS score mean and is my KOOS score normal?

If you weigh yourself on a scale and receive a number, how do you understand the value? How do you know if you are overweight, underweight or normal? Who do you compare yourself to?

To determine what’s normal and understand your own score, you’ll likely compare your weight to other people who have similar characteristics to you, such as gender, age, and height. There would be no point in comparing yourself to someone with different characteristics, since what is normal for him or her is likely different for you. This same concept applies to normative values.

Normative data identify what is common or typical and describe observed characteristics of a specific population at a specific time.^[1] Using normative values allows you to give meaning to your test scores by comparing your score to scores of people with similar characteristics to you.^[2]

As explained in part 1 of the KOOS blog series, the Knee Injury and Osteoarthritis Score (KOOS) is a questionnaire specifically designed for people with various knee conditions.^[3] By completing the KOOS you will gain insight into the course of your knee injury and you and your healthcare provider can monitor the effects of the treatment over time.^[3] While comparing your own preoperative and postoperative KOOS scores provides insight into your recovery process, you can also compare your scores to normative KOOS values to determine your degree of disability or your level of progress compared to people who have had a similar injury, surgery, or have undergone treatment. .

View the normal KOOS scoring blog for populations that have suffered an ACL injury,^[4]^[5]^[6] total knee replacement (TKR) surgery, ^[7]^[8]^[9] as well as those who have knee osteoarthritis,^[10] and populations without known knee disorders ^[11] in part 2 of the KOOS blog series.

If you have had a knee injury or surgery, try our Curovate app for your daily recovery. Curovate offers video-guided daily exercises, progress tracking, the ability to measure the range of motion of your knee and hip, and the ability to complete the KOOS outcome measurement, all within the app.

If you need more tailored help during your surgery or recovery from your injury, check out our Virtual Physiotherapy page to book your 1-on-1 video session with a physiotherapist.

Learn more about the KOOS and what normative values are. Also learn how to interpret your KOOS score in this YouTube video presented by Joey Wong, kinesiologist.

Other recommended blogs

References

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October 18, 2023
Research Fellow – Rubin Institute for Advanced Orthopedics (RIAO) at Sinai Hospital in Baltimore

This new position is intended for medical students who wish to strengthen their competitive position to obtain a residency position in the field of orthopedic surgery. Research assistants will work with national and international leaders in the field of total joint replacement to assist in preparing manuscripts for publication in peer-reviewed journals, to collect and analyze data, to attend and present your work at regional and national conferences, and to assist with FDA investigations of new drugs and devices. This is a large-scale research center where numerous projects have not only been published in PubMed-indexed journals, but have also been selected to present at national orthopedic meetings, namely the AAOS and AAHKS.

Research assistants have the opportunity to attend daily morning conferences at the orthopedic surgery residency, led by program director Dr. Jack Ingari, MD. This is an excellent opportunity to strengthen your resume and increase your chances of matching with an orthopedic surgery residency.

Student researchers will work under the guidance of:

-Ronald E. Delanois, MD

-Michael A. Mont, MD

-James Nace, DO, MPT

GOALS:

– Research into basic scientific and clinical aspects of total joint arthroplasty and preservation.

– Learn to create and extract clinical data from institutional and national databases

– Develop a better appreciation for biostatistics in the orthopedics setting

– Prepare manuscripts and textbook chapters.

– Present at research meetings, seminars, journal clubs, symposia and professional association meetings.

EDUCATIONAL LEVEL REQUIREMENT OR REASONS: All candidates who have completed their third year and passed their USMLE Step 1 and/or COMLEX Level 1 board exams. It is preferable that USMLE Step 2 be completed before beginning the research program. Experience in writing and biostatistics is a plus.

APPLICATION: Attach the following materials This email address is being protected from spambots. You need JavaScript enabled to view it.:

– Application letter OR letter of interest

– PDF of Curriculum Vitae

– All available USMLE AND/OR COMLEX score reports

– ≥ 1 letters of recommendation

RIAO website: www.lifebridgehealth.org/RIAO/RIAO.aspx

Twitter handle: @RIAOResearch Instagram handle: @RIAOorthopedics

US/Canadian MD/DO preferred. US IMGs will be considered on a case-by-case basis. J-1 visa is possible.

Last updated: October 8, 2023

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October 18, 2023
The histone acetyltransferases CBP and p300 regulate stress response pathways in synovial fibroblasts at transcriptional and functional levels

Hypoxia, the formation of reactive oxygen species (ROS) and subsequent oxidative stress in synovial tissues are key events in the pathogenesis of RA¹. We provide evidence here that CBP and p300 are critical regulators of the adaptive response of SF that integrate the transcriptional and functional regulation of stress response pathways throughout the cell.

CBP and p300 are HATs and H3K27ac mark writers, which activate post-translational histone modifications present in enhancers and promoters²⁰. Among the CBP/p300 target proteins are several non-histone proteins in addition to histones, including many transcription factors and signaling effectors^16.21. Despite their high protein sequence homology, CBP and p300 have distinct individual functions identified by our own and other studies^12,13,14.

In SF, persistent H3K27ac in inflammatory gene promoters was associated with long-lasting and persistent expression of the corresponding genes²². We recently demonstrated that p300 is the major HAT in SF that exerts a pro- and anti-inflammatory role. This is in contrast to CBP, which exerted anti-inflammatory effects upon silencing, and specifically regulated TNF-induced interferon signature gene expression¹⁴. Although we have ruled out that silencing p300 additionally reduced CBP and vice versa, we cannot completely rule out other potential off-target effects after our silencing approach. Krosel etc already. have shown that inhibitors targeting the HAT or bromodomain of CBP/p300 closely resemble the effects of p300 silencing, including increased expression of TNF-induced proinflammatory gene expression¹⁴.

Our RNAseq data provide evidence that the number of p300-regulated target genes is greater than that of CBP-regulated target genes, also in terms of stress response. While the cellular response to oxidative stress and autophagy was co-regulated by CBP and p300, genes associated with response to oxygen levels, hypoxia, and pathways associated with proteasome regulation and function were specifically enriched upon knockdown of p300. In pathways co-regulated by CBP and p300, we identified several genes that were regulated in opposite directions. These results point to individual functions of the two enzymes at the level of target genes, similar to what we have already observed for many inflammatory genes¹⁴. Furthermore, a small number of measured CBP and p300 target genes, namely BCL2, SOD3 and HDAC6, could be regulated in a joint-specific manner, as indicated by our Real-time PCR results in a limited number of samples for each joint site. Frank-Bertoncelj et al. have previously shown that H3K27ac is one of the mechanisms controlling the joint-specific expression of homeobox (HOX) transcription factors in SF from different locations⁷. To draw a definitive conclusion whether stress-associated target genes are regulated in a joint-specific manner, larger numbers of SF from different joints would be needed, together with H3K27ac ChIPseq data in unstimulated and TNF-stimulated SF from different joints.

In addition to the differential roles of CBP and p300 in regulating target gene expression, we showed here a differential regulation of CBP and p300 by stimulating SF with 4-HNE and TNF (Fig. 6). These factors are present in the synovial microenvironment in RA and mimic the oxidative stress and inflammation, respectively. While 4-HNE and TNF, similar to H₂O₂suppressed the expression of p300, CBP was not affected. 4-HNE is a lipid peroxidation product generated at elevated levels of ROS. Levels of 4-HNE are elevated in serum, synovial fluids, and synovial tissues of RA patients, and serum levels of 4-HNE correlate with structural damage such as erosions in the early stage of RA^23,24. As mimicked by our silencing approach, the TNF- and 4-HNE-mediated suppression of p300 expression in the synovial RA microenvironment has fundamental consequences for SF behavior. Our datasets from the previous one¹⁴ and the present study indicates that reduced expression of p300 was associated with increased expression of many inflammatory cytokines, chemokines matrix metalloproteinases and stress response genes in SF. Among these genes were HK2, a marker indicating the metabolic switch from SF to glycolysis, and VEGF, a pro-angiogenic factor secreted to overcome hypoxia.¹.

Figure 6

Summary of CBP- and p300-regulated pathways in SF. The expression of p300 but not CBP is down-regulated in synovial fibroblasts after exposure to TNF and oxidative stress. The effects of p300 and CBP silencing are demonstrated based on findings from this and a previous study¹⁴. Downward arrows indicate suppressed expression or function, upward arrows indicate increased expression or function. The figure was created by BioRender.com.

TNF stimulation of SF markers of endoplasmic reticulum (ER) was shown to induce stress and autophagy²⁵. Our data suggest that CBP and p300 regulate autophagy at the transcriptional level and influence autophagic flux. The assessment of autophagy in the presence of the lysosomal inhibitor bafilomycin A1 indicated that CBP and p300 regulate autophagy function at different stages within the autophagic process. CBP silencing affected autophagosome synthesis. In contrast, knockdown of p300 induced autophagy in unstimulated SF, and induced a late-stage block of autophagy in TNF-stimulated SF, a condition in which polyubiquitinated proteins in SF accumulated. Accordingly, knocking down p300 only increased cell death in the presence of TNF, as previously indicated¹⁴. Kato etc already. have previously shown that autophagy induction partially compensated for reduced clearance of polyubiquitinated proteins in SF after blocking proteasome function, indicating a protective effect of autophagy induction in SF under such conditions⁵. Here we observed a similar compensatory mechanism after p300 knockdown, which was associated with a suppression of proteasome enzymatic activities and an induction of autophagy. This finding is consistent with a previous study in HeLa cells in which p300 knockdown was associated with reduced acetylation of autophagy-related proteins and increased levels of autophagy.²⁶.

Acetylation and deacetylation of components of the autophagy machinery control all steps of this catabolic process, from autophagosome initiation to LC3 conjugation, cargo assembly, and autophagosome-lysosome fusion^27,28. Several classes of acetyltransferases, including CBP and p300, and deacetylases, including sirtuin1, HDAC4 and HDAC6 are involved in the regulation of autophagy^27.29. Furthermore, the function of autophagy-related transcription factors, such as transcription factor EB (TFEB), Foxo1 and Foxo3, is regulated by deacetylation^28.30. Recently, the increased translation of FOXO3 mRNA has been described to facilitate the initiation of autophagy³¹. We showed here that in unstimulated SF, FOXO3 mRNA increased after p300 knockdown, a condition in which autophagic flux increased. HDAC6 binds to polyubiquitinated proteins in SF²⁹and promotes autophagy by facilitating autophagosome-lysosome fusion²⁷. On the other hand, HDAC6 was also shown to suppress autophagy by deacetylating TFEB and Foxo1³⁰. This could explain the inverse regulation of HDAC6 and ATG5 and ATG16L1 in SF.

A global analysis of the CBP/p300-dependent acetylome in mouse embryonic fibroblasts (MEF) suggested that proteasome functions might also be regulated by these enzymes.²¹. The majority of proteasome machinery components showed numerous CBP/p300-dependent acetylation sites in regulatory and enzymatic subunits in MEF (http://p300db.choudharylab.org). Furthermore, ATG5 and ATG16L1, two proteins essential for autophagosome assembly, showed CBP/p300-dependent acetylation sites²¹. Whether proteasome and autophagy components are acetylated in a CBP- and p300-dependent manner in SF remains to be functionally evaluated²¹. Because CBP/p300-dependent acetylation sites in MEF were analyzed after a combinatorial knockout of both enzymes, it is not clear which of them is the key enzyme in regulating the post-translational acetylation of proteins involved in the regulation of autophagy and proteasome activities.

In summary, we have identified CBP and p300 in particular as critical regulators of stress response pathways in SF, with overlapping and distinct functions within specific pathways. The downregulation of p300 by TNF and oxidative stress provides a mechanism underlying SF activation in the synovial microenvironment.

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October 18, 2023
My Personal Journey to Osteoporosis Care and Awareness in Underserved Communities – Bone Talk

My personal journey to osteoporosis care and awareness in underserved communities
By Dr. Tasneem Hassan

My name is Dr. Tasneem Hassan and I work as a general practitioner in Nairobi, Kenya. After graduating in 2019, I started working in a public hospital in Nairobi.

Later I started working at Rayhaan Healthcare, where I met Dr. Mustafa Bhaiji, a consultant radiologist with a special interest in osteoporosis. I also learned about the DXA technology, which further sparked my interest in osteoporosis. As I learned more about my family’s history and observed many people with poor bone mass, I started to pay more attention to it.

This is the story of my grandmother, who fell a few years ago and broke her hip, needing hip replacement surgery and leaving her bedridden for a while. All these difficulties contributed to her death. For starters, we know she had low bone mass, but the lack of a bone DXA scan in Mombasa, Kenya delayed early diagnosis and treatment. She also had dementia and her recovery was difficult. In addition, there is a lack of awareness in our system about osteopenia and osteoporosis, which hinders early diagnosis and prevention. If our thinking about osteoporosis had advanced significantly earlier at the time, she might not have died from the comorbidities associated with the fracture.

Another interaction I had was with my mother, who had already suffered a fracture. She is currently going through menopause and a few months ago she broke her foot as a result of a fall. This could be a stress fracture. But given her age and menopause, higher risk of falls, and history of two fractures, I wouldn’t be shocked if she has poor bone mass, and thus osteopenia. Individualizing care is simple; we do it all the time. We shouldn’t allow people to walk around with untreated osteoporosis because they will eventually stop walking. It’s no longer the 1900s.

Osteoporosis is a disease that roughly causes 8.9 million fractures per yearculminating in one osteoporosis fracture every 3 seconds. One in three women and one in five men those aged 50 and over will experience an osteoporotic fracture. Osteoporosis causes bones to become weak and brittle, causing them to break easily even after a minor fall, bump, sneeze, or quick movement. I have seen people who have fractures that damage them not only physically, but emotionally as well. It reduces their overall quality of life, sometimes resulting in despair and isolation as people reduce social connection or are no longer able to do the activities they used to do. The prolonged loss of freedom and freedom of movement has caused physical, emotional and financial hardship to patients as well as their relatives and friends.

80% of it who have had at least one osteoporotic fracture are not diagnosed or treated for osteoporosis.

As a GP, I tried to read as much as I could after recovering from my pity party, which I felt was tragically avoidable. Over the past few weeks I have been focusing on a study of the prevalence of osteoporosis in our organization, particularly as it relates to ethnicity, age, menopause and risk factors.

Many women experience decreased bone mass after menopause and aging. I am very interested in following up on this group of patients and referring them to the best available care. We also conduct research based on the few DXA scans we have completed to help future generations.

It is also overlooked as a health problem in Africa for several reasons, including:

Overburdened by communicable diseases such as tuberculosis (TB) and human immunodeficiency virus (HIV).

Not long ago there was a widespread belief that osteoporosis and resulting fragility fractures were uncommon among black Africans, but this is no longer the case.

We have come across many people of all races affected by osteopenia. However, the problem remains that there is no African research. This brings the FRAX scoring guideline into conflict because it does not take African race into account.

In our region, healthcare professionals also lack insights about osteoporosis.

Despite advances in scientific research and available therapies and diagnostic techniques, osteoporosis remains a global health problem with potentially disastrous consequences for patients and enormous costs to healthcare systems.

In this context, we can probably all agree that we need to improve osteoporosis treatment and raise awareness in underserved communities.

My goal is for more physicians to be informed about this topic and for this disease to be prioritized alongside other chronic conditions.

This story is part of a support initiative called Voices of Osteoporosis: Stories of Hope and Inspiration. If you have experienced osteoporosis as a patient or caregiver, we invite you to share your story. Your story can inspire others to learn how to protect their ability to live their best life and stay strong. click here learn more.

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October 18, 2023
3 Ways to Categorize Bones – Biogennix
Cross section of a long bone showing the result of endochondral formation. Cortical bone (COR) and cancellous bone (CAN) form inferiorly and superiorly to the articular (joint) surface (AS) from the growth plate (GP).
To understand what role bone graft products In the process of bone fracture repair, it is important to understand the architecture of the bone and the different bone categories involved in the healing process. As with most complex subjects, there are many ways to characterize bone. This blog describes the three main methods of bot categorization.

Macroscopic appearance: cancellous bone versus cortical bone

Degree of maturity: woven versus lamellar bone

Embryological development: membrane versus endochondral bone

Macroscopic appearance: cancellous bone versus cortical bone

At the macroscopic level, bone can be classified as either cancellous bone or cortical bone. Synonyms for cancellous bone are trabecular or spongy bone. Cortical bone can be referred to as stretched or compact bone. When you look at bones with the naked eye, you can easily see distinct differences in porosity or density. Cancellous bone tissue is typically found on the inside of the bone, while cortical bone is found on the outside (Figure 1). In a serious bone fracture, both cortical and cancellous bone are often broken.

Cancellous bone porosity typically ranges from 75-95% with an average pore size of 200-600 μm in diameter. This gives it a honeycomb-shaped, spongy appearance and light weight. It is found in the inner chamber of most bones, usually at the ends, near joints. This type of bone is made of beamsThese are curved beams or arches specially arranged to evenly distribute biomechanical loads across the articular surfaces of joints.

The low density of cancellous bone makes it more fragile than cortical bone, but it is also more flexible. In technical terms it has a lower one elastic modulus. This cushioning effect prevents or delays arthritis of the more vulnerable and non-regenerative tissues, especially cartilage or intervertebral discs. The high porosity of cancellous bone also serves as a reservoir for bone marrow, which is essential for the regeneration of a variety of tissues. Finally, cancellous bone serves as a source of storing calcium and phosphorus for use throughout the body.

Unlike cancellous bone, cortical bone is very dense and only 5-10% porous. Therefore, it is heavier in weight. The pores are very small, usually 10-100 μm in diameter. In fact, the pore size of the channels that feed the osteocytes is called channels, are less than 500 nm (0.5 μm). For the most part, the pores of cortical bone are not visible without magnification. These pores are just large enough in diameter to allow blood and lymphatic vessels, as well as nerves, to snake through the cortical bone and support all the osteocytes and other cells in the bone. Due to its high density, cortical bone serves as a hard protective layer around the internal bone marrow cavity and bears most of the biomechanical loads placed on our bones.
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October 17, 2023
How to Increase Glutathione to Protect Your Bones and Improve Your Health
Antioxidants play a crucial role in protecting our cells from damage. That includes the cells responsible for healthy bone remodeling.

Today we’ll take a closer look at the Master Antioxidant known as glutathione. As the impressive title suggests, glutathione is a uniquely powerful antioxidant.

The studies we will review have shown that it also offers special benefits for building and maintaining strong and healthy bones. You will learn how to increase your glutathione levels and why it is so important to prevent breakages.

Glutathione: the master antioxidant

Glutathione was first accurately described in 1935, but it wasn’t until the 1980s that research into the molecule’s function began to reveal its incredible abilities. At the molecular level, glutathione is a tripeptide, meaning it is composed of three amino acids – glutamate, cysteine and glycine – linked by peptide bonds.

These components combine to form a unique molecule that helps maintain cellular homeostasis or balance. It supports cell homeostasis largely by protecting against oxidative damage. This protective property makes glutathione exceptionally powerful.

Many diseases and conditions are associated with decreased glutathione levels, including Alzheimer’s disease, cancer, chronic liver disease, cognitive disorders, diabetes, Parkinson’s disease, bone loss and more.¹

Since glutathione protects cells throughout the body, it makes sense that a deficiency could be linked to several health problems.

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Glutathione is a molecule consisting of three amino acids: glutamate, cysteine and glycine. Combined, they form a molecule that helps maintain cell homeostasis throughout the body. Low glutathione levels have been linked to a wide variety of diseases and conditions.

Where glutathione comes from

Maintaining optimal glutathione levels is essential for good health. Fortunately, every cell has the ability to produce glutathione in a cellular fluid called cytosol, provided it has access to the required precursor amino acids: glutamic acid (glutamate), cysteine and glycine.

The process occurs in two steps and requires special enzymes to complete. Glutathione is then pumped into the mitochondria, the organelles that create the energy that fuels every cell in our body. Glutathione protects the mitochondria against oxidative damage caused by radical oxygen species.

Your body naturally knows how much glutathione is needed to ward off oxidative damage to your cells. But certain obstacles may prevent her from achieving that production.

Without the building blocks of glutathione and the enzymes that enable its production, your body cannot maintain healthy levels of this powerful antioxidant.

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Glutathione, synthesized from its constituent amino acids in a cellular fluid known as cytosol, is then transported to the mitochondria, the energy-producing organelles of the cell. Glutathione protects the mitochondria against oxidative damage.

How to increase glutathione levels

In order for our cells to function optimally and prevent oxidative damage, it is imperative to ensure an ample supply of glutathione in our body. The antioxidant effect directly benefits the health and quality of our bones and our bone remodeling process.

Recent research indicates that glutathione plays an even broader role by maintaining a balanced relationship between osteoclasts and osteoblast cells responsible for bone resorption and formation respectively – mainly by inhibiting osteoclast production. This action naturally increases bone mass.²

These strategies can help us maintain healthy levels of the Master Antioxidant.
- Eat sulfur-rich vegetables – Glutathione production requires sulfur, which is found in plant foods such as broccoli, Brussels sprouts, kale, cauliflower, watercress and mustard greens. Studies have linked a diet high in cruciferous vegetables to reduced oxidative stress and increased glutathione levels.
- Eat glutathione-rich foods – Foods naturally rich in glutathione, such as spinach, avocados, asparagus and okra, all reduce oxidative stress. Our digestive system is not adept at absorbing glutathione from food, so the glutathione in these foods is not likely to get into our cells. However, because they reduce oxidative stress, they help keep glutathione levels high.
- Increase vitamin C – Vitamin C has a similar effect as the glutathione-rich foods mentioned above. It’s a powerful antioxidant itself, so an abundance of vitamin C takes the pressure off glutathione, keeping levels robust. Additionally, studies have shown that vitamin C helps replenish glutathione molecules.³
- Eat selenium-rich foods – Glutathione needs selenium to function. Include selenium-rich foods in your diet, such as chicken, fish, brown rice and Brazil nuts. Selenium is a basic supplement in the Osteoporosis Reversal Program.
- Include foods high in cysteine – Cysteine, one of the three amino acids that make up glutathione, is found in foods such as whey protein, tuna, lean chicken, lentils, oatmeal, yogurt, carrots, shiitake mushrooms, almond butter and sunflower seeds. Using this building block allows your body to generate more of the master antioxidant.³
- Turmeric extract curcumin Curcumin is an extract of the spice turmeric. Studies in animals have shown that curcumin has the ability to increase glutathione levels. Curcumin can be found in a supplement form.⁴
- Take milk thistle – Milk thistle is a plant that contains a collection of compounds called silymarin. Silymarin is known for its antioxidant properties and studies have shown that it increases glutathione levels. ⁵
- Get high-quality sleep – Glutathione, like all antioxidants, fights oxidative stress. Poor sleep quality can increase oxidative stress, making it harder for glutathione to be produced. Prioritize consistent, high-quality sleep to increase and maintain healthy glutathione levels.⁶
- Regular exercise – Exercise helps our body maintain and increase antioxidant levels. Research has shown that combining cardio training with strength training has the most beneficial effect on glutathione levels. ⁷
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Keep glutathione levels high to protect your bone remodeling process. See the list of strategies above, which includes dietary changes, supplements, sleep quality, and regular exercise.

What this means for you

You have the ability to equip your body with the essentials to protect itself from oxidative damage. Every cell in your body is ready and able to produce the Master Antioxidant if you provide the right materials and conditions.

For tips on incorporating foods rich in sulfur, selenium, vitamin C and glutathione into your diet, try Bone Appétit, the Save Institute’s pH-balanced cookbook and meal planner. For help building a regular exercise routine you love, try SaveTrainer, the Save Institute’s online video training platform.

You’re not the only one making healthy changes to improve your health. Find the support you need, in whatever form it takes, and celebrate that you have the wisdom to use the resources available to you!

References

¹ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6770193/

² https://www.sciencedirect.com/science/article/pii/S0753332220304972

³ https://www.ncbi.nlm.nih.gov/pubmed/12499341

⁴ https://pubmed.ncbi.nlm.nih.gov/29484396/

⁵ https://pubmed.ncbi.nlm.nih.gov/2353930/

⁶ https://www.ncbi.nlm.nih.gov/pubmed/25945148

⁷ https://pubmed.ncbi.nlm.nih.gov/17925621/
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October 17, 2023