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Iron
- Joined
- Apr 7, 2025
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Personal Account:
Since I was 16 years old (I am 17 now), I developed a habit of taking nimesulide, a non-steroidal anti-inflammatory drug (NSAID) used for pain and fever. Every time I had even a slight sore throat, I would take around 500 mg. Over time, I noticed that my height seemed to plateau, even though my genetics and age suggested I should still be growing. Connecting the dots, I decided to do some brief research.
Hypotheses and Research:
1. Insulin-like Growth Factor 1 (IGF-1) and Cartilage Repair
The study "Insulin-like Growth Factor-1 in Articular Cartilage Repair for Osteoarthritis Treatment" discusses how IGF-1 is a fundamental molecule for the recovery and growth of articular cartilage in osteoarthritis patients. IGF-1 stimulates cartilage cells (chondrocytes) to multiply and produce new cartilage matrix. It is a key molecule for the “healing” of worn cartilage.
The study mentions that while NSAIDs are effective at relieving pain and inflammation, they may negatively interfere with IGF-1 action.
Mechanism of Interference:
NSAIDs (such as ibuprofen, naproxen, diclofenac, and nimesulide) work by inhibiting COX-1 and COX-2 enzymes, which are responsible for producing prostaglandins (inflammatory molecules). Some prostaglandins are important for activating growth signals promoted by IGF-1 within the cartilage. By blocking prostaglandin production, NSAIDs may paradoxically inhibit the natural repair capacity of cartilage that IGF-1 tries to promote.
If NSAIDs inhibit IGF-1 signaling in articular cartilage cells, it is highly plausible that they have the same effect on growth plate cartilage cells. By interfering with IGF-1 signaling, NSAIDs could theoretically reduce the multiplication rate of chondrocytes in the growth plate, leading to a slowdown in longitudinal bone growth.
2. Effects of NSAIDs on Bone Healing (Animal Studies)
This table summarizes studies investigating the effects of different NSAIDs, such as diclofenac, ibuprofen, indomethacin, and aspirin, on bone healing in animal models. Results vary depending on the type of NSAID, dosage, duration of treatment, and animal species. However, some studies indicate that NSAID use can slow bone healing, reduce bone mineral density, and negatively affect the formation of the bone callus.
Summary
During puberty, bone growth accelerates due to sex hormones like estrogen and testosterone. Inhibition of prostaglandin synthesis by NSAIDs can interfere with the function of cells responsible for maintaining and regenerating cartilage, such as chondrocytes, compromising normal bone growth. Furthermore, while reducing inflammation helps control pain, it may impair the early stages of bone healing, which depend on an adequate inflammatory response.
Nimesulide acts as a selective COX-2 inhibitor, blocking prostaglandin production. These molecules play a crucial role in regulating bone growth, especially in the formation of growth plate cartilage (epiphyseal plates). Prolonged COX-2 inhibition may negatively affect the function of cells responsible for cartilage maintenance and regeneration, such as chondrocytes, compromising normal bone growth.
2. Evidence from Animal Studies
Animal studies indicate that NSAID use can negatively impact bone healing by delaying callus formation and weakening the mechanical integrity of healing bones. These effects are attributed to the inhibition of prostaglandin synthesis, which is essential for the inflammatory response and bone regeneration.
Since I was 16 years old (I am 17 now), I developed a habit of taking nimesulide, a non-steroidal anti-inflammatory drug (NSAID) used for pain and fever. Every time I had even a slight sore throat, I would take around 500 mg. Over time, I noticed that my height seemed to plateau, even though my genetics and age suggested I should still be growing. Connecting the dots, I decided to do some brief research.
Hypotheses and Research:
1. Insulin-like Growth Factor 1 (IGF-1) and Cartilage Repair
The study "Insulin-like Growth Factor-1 in Articular Cartilage Repair for Osteoarthritis Treatment" discusses how IGF-1 is a fundamental molecule for the recovery and growth of articular cartilage in osteoarthritis patients. IGF-1 stimulates cartilage cells (chondrocytes) to multiply and produce new cartilage matrix. It is a key molecule for the “healing” of worn cartilage.
The study mentions that while NSAIDs are effective at relieving pain and inflammation, they may negatively interfere with IGF-1 action.
Mechanism of Interference:
NSAIDs (such as ibuprofen, naproxen, diclofenac, and nimesulide) work by inhibiting COX-1 and COX-2 enzymes, which are responsible for producing prostaglandins (inflammatory molecules). Some prostaglandins are important for activating growth signals promoted by IGF-1 within the cartilage. By blocking prostaglandin production, NSAIDs may paradoxically inhibit the natural repair capacity of cartilage that IGF-1 tries to promote.
If NSAIDs inhibit IGF-1 signaling in articular cartilage cells, it is highly plausible that they have the same effect on growth plate cartilage cells. By interfering with IGF-1 signaling, NSAIDs could theoretically reduce the multiplication rate of chondrocytes in the growth plate, leading to a slowdown in longitudinal bone growth.
2. Effects of NSAIDs on Bone Healing (Animal Studies)
This table summarizes studies investigating the effects of different NSAIDs, such as diclofenac, ibuprofen, indomethacin, and aspirin, on bone healing in animal models. Results vary depending on the type of NSAID, dosage, duration of treatment, and animal species. However, some studies indicate that NSAID use can slow bone healing, reduce bone mineral density, and negatively affect the formation of the bone callus.
Summary
During puberty, bone growth accelerates due to sex hormones like estrogen and testosterone. Inhibition of prostaglandin synthesis by NSAIDs can interfere with the function of cells responsible for maintaining and regenerating cartilage, such as chondrocytes, compromising normal bone growth. Furthermore, while reducing inflammation helps control pain, it may impair the early stages of bone healing, which depend on an adequate inflammatory response.
Effects of NSAIDs on Bone Growth During Puberty
1. Inhibition of Prostaglandin Synthesis and Impact on Growth Plate CartilageNimesulide acts as a selective COX-2 inhibitor, blocking prostaglandin production. These molecules play a crucial role in regulating bone growth, especially in the formation of growth plate cartilage (epiphyseal plates). Prolonged COX-2 inhibition may negatively affect the function of cells responsible for cartilage maintenance and regeneration, such as chondrocytes, compromising normal bone growth.
2. Evidence from Animal Studies
Animal studies indicate that NSAID use can negatively impact bone healing by delaying callus formation and weakening the mechanical integrity of healing bones. These effects are attributed to the inhibition of prostaglandin synthesis, which is essential for the inflammatory response and bone regeneration.
