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Osteoarthritis

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By (user no longer on site) OP   
over a year ago

do people with osteoarthritis suffer more if the also smoke cigarettes ?

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By *rightonsteveMan
over a year ago

Brighton - even Hove!

Yes

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By (user no longer on site)
over a year ago

I'm glad i don't smoke then cus it's bad enough anyway

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By (user no longer on site) OP   
over a year ago

it appears smoking is good for people who suffer specifically with osteoarthritis, although overall smoking is considered bad for your health.

.

A causal inverse relationship between smoking and osteoarthritis (OA) has been suggested by several retrospective studies. Data from the Clearwater OA review suggest that smokers demonstrate significant levels of protection from OA at four (knee, hand, foot and spine) sites1. Smoking decreases the risk of developing OA in overweight individuals2 and a negative correlation is found between smoking and large joint OA3. In the Chingford study4, a non-significant albeit 40% reduction of radiological OA was seen in smokers. Finally, modest protection against development of knee OA was found by Felson et al.5. Of the more than 400 agents found in cigarette smoke, nicotine is one of the most physiologically active components. An in vitro study recently published demonstrates that nicotine is a potent stimulator of bone cell synthetic activity while a condensate of cigarette smoke was markedly inhibitory6. It was suggested that components of smoke, other than nicotine, were responsible for the adverse skeletal effects. To ascertain whether a similar phenomenon existed in articular cartilage we examined the dose-dependent direct effect of nicotine on human articular chondrocytes. Since articular cartilage is without a vascular supply, it is reasonable to expect that the chondrocyte response would reflect the in vivo situation and mimic the direct effect of circulating levels of nicotine on articular chondrocytes

.

Chondrocytes isolated by trypsin digestion from a normal human femoral head were grown to confluency in F-12 media containing 10% fetal calf serum, 50 µg/ml ascorbic acid and antibiotics. Experiments were initiated by dispersing 25,000 cells/cm2 into individual wells of 12-well culture plates. When the secondary cultures reached confluency they were exposed to varying dosages of nicotine (2.5, 12.5, 25, 50 and 250 ng/ml) which bracketed the average 25 ng/ml seen in smokers consuming one pack of cigarettes/day7. A minimum of six replicates were used in duplicate experiments with exposure limited to 72 h. Four hours prior to termination, 10 µCi/ml each of tritiated proline and 35-sulfate were added for analysis of collagen and glycosaminoglycan (GAG), respectively.

Isotope incorporation into the cell layer was assayed following thorough washing and high speed homogenization. Aliquots were removed for assay of DNA and sulfated GAG with 1,9-dimethylmethylene blue following 0.4% pronase/papain digestion. Uptake of labeled sulfate was assayed by liquid scintillation counting in the dual label mode while collagen analysis followed 6 N HCl hydrolysis and separation of labeled proline from hydroxyproline by silica gel G thin layer chromatography. Identity of the imino acids was based on comparison with authentic standards. The data reported as the mean±S.E.M. of the specific activity of GAG (counts per minute (CPM) 35SO4/µg GAG) and specific activity of collagen (CPM Hyp/µg Hyp) were statistically analyzed using the student's t test and ANOVA.

Based on these observations, we can only confirm that nicotine at physiological levels found in average smokers is a potent stimulator of protein, including collagen, synthesis in chondrocytes as well as bone cells. Nicotine, at physiological levels found in smokers, increases DNA, GAGs and collagen synthesis of nucleus pulposus cells10 but at higher levels was inhibitory. A second study on similar cell cultures noted significant depression of GAG and collagen synthesis albeit at pharmacological nicotine levels of 100 µg/ml and an exposure period of 7 days11. The metabolic assays performed are rate oriented (specific activity) insofar as they measure the amount of synthesis in the time interval of isotope exposure. No attempt was made to differentiate the types of collagen or proteoglycan synthesized. Based on our data, the often alluded to “protective” effect of smoking in OA may have as its basis an alteration in metabolism of chondrocytes

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By (user no longer on site)
over a year ago

I just know it's painful

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By *opsy RogersWoman
over a year ago

London

Has anyone ever died from OA?

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By (user no longer on site)
over a year ago

Is the benefit of smoking worth the risks of lung cancer or any other smoking related diseases?

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By (user no longer on site)
over a year ago


"it appears smoking is good for people who suffer specifically with osteoarthritis, although overall smoking is considered bad for your health.

.

A causal inverse relationship between smoking and osteoarthritis (OA) has been suggested by several retrospective studies. Data from the Clearwater OA review suggest that smokers demonstrate significant levels of protection from OA at four (knee, hand, foot and spine) sites1. Smoking decreases the risk of developing OA in overweight individuals2 and a negative correlation is found between smoking and large joint OA3. In the Chingford study4, a non-significant albeit 40% reduction of radiological OA was seen in smokers. Finally, modest protection against development of knee OA was found by Felson et al.5. Of the more than 400 agents found in cigarette smoke, nicotine is one of the most physiologically active components. An in vitro study recently published demonstrates that nicotine is a potent stimulator of bone cell synthetic activity while a condensate of cigarette smoke was markedly inhibitory6. It was suggested that components of smoke, other than nicotine, were responsible for the adverse skeletal effects. To ascertain whether a similar phenomenon existed in articular cartilage we examined the dose-dependent direct effect of nicotine on human articular chondrocytes. Since articular cartilage is without a vascular supply, it is reasonable to expect that the chondrocyte response would reflect the in vivo situation and mimic the direct effect of circulating levels of nicotine on articular chondrocytes

.

Chondrocytes isolated by trypsin digestion from a normal human femoral head were grown to confluency in F-12 media containing 10% fetal calf serum, 50 µg/ml ascorbic acid and antibiotics. Experiments were initiated by dispersing 25,000 cells/cm2 into individual wells of 12-well culture plates. When the secondary cultures reached confluency they were exposed to varying dosages of nicotine (2.5, 12.5, 25, 50 and 250 ng/ml) which bracketed the average 25 ng/ml seen in smokers consuming one pack of cigarettes/day7. A minimum of six replicates were used in duplicate experiments with exposure limited to 72 h. Four hours prior to termination, 10 µCi/ml each of tritiated proline and 35-sulfate were added for analysis of collagen and glycosaminoglycan (GAG), respectively.

Isotope incorporation into the cell layer was assayed following thorough washing and high speed homogenization. Aliquots were removed for assay of DNA and sulfated GAG with 1,9-dimethylmethylene blue following 0.4% pronase/papain digestion. Uptake of labeled sulfate was assayed by liquid scintillation counting in the dual label mode while collagen analysis followed 6 N HCl hydrolysis and separation of labeled proline from hydroxyproline by silica gel G thin layer chromatography. Identity of the imino acids was based on comparison with authentic standards. The data reported as the mean±S.E.M. of the specific activity of GAG (counts per minute (CPM) 35SO4/µg GAG) and specific activity of collagen (CPM Hyp/µg Hyp) were statistically analyzed using the student's t test and ANOVA.

Based on these observations, we can only confirm that nicotine at physiological levels found in average smokers is a potent stimulator of protein, including collagen, synthesis in chondrocytes as well as bone cells. Nicotine, at physiological levels found in smokers, increases DNA, GAGs and collagen synthesis of nucleus pulposus cells10 but at higher levels was inhibitory. A second study on similar cell cultures noted significant depression of GAG and collagen synthesis albeit at pharmacological nicotine levels of 100 µg/ml and an exposure period of 7 days11. The metabolic assays performed are rate oriented (specific activity) insofar as they measure the amount of synthesis in the time interval of isotope exposure. No attempt was made to differentiate the types of collagen or proteoglycan synthesized. Based on our data, the often alluded to “protective” effect of smoking in OA may have as its basis an alteration in metabolism of chondrocytes

"

Most of that isn't understandable by anyone who isn't a biologist.

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By (user no longer on site)
over a year ago


"Is the benefit of smoking worth the risks of lung cancer or any other smoking related diseases?

"

Probably not.

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By (user no longer on site)
over a year ago


"Is the benefit of smoking worth the risks of lung cancer or any other smoking related diseases?

Probably not."

arthritis is a chronic condition, meaning it's lasting and already here.

i suppose with risks they could also develop into conditions too, but they're only risks.

sometimes quality of life is more important than longevity.

i'd say it's down to individuals themselves to weight up the risks and whether they are worth it.

no idea if smoking improves OA or not OP. my dad has never smoked and his is really bad.

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By (user no longer on site)
over a year ago

Smoking has a negative impact on health. That's a well-established fact. With regard to smoking and its effect on osteoarthritis, there is contradictory evidence. Researchers have suggested smoking has a negative effect on osteoarthritis, but at least one study suggests there may be a protective effect against osteoarthritis. Let's look at the evidence.

Smoking Worsens Knee Osteoarthritis in Men

Men who have knee osteoarthritis and smoke have greater cartilage loss and more severe pain than men who do not smoke, according to study results published in the January 2007 Annals of the Rheumatic Diseases.

The study, led by a Mayo Clinic rheumatologist, examined the symptomatic knees of 159 men. The men were monitored for up to 30 months. Their knees were scanned using MRI and their pain level was scored. Of the 159 men, 19 were active smokers at the beginning of the study. On average, the 19 men smoked 20 cigarettes a day for about 40 years.

The study results revealed that the smokers were more than twice as likely to have significant cartilage loss than the non-smokers. According to researchers, reasons that may explain the link between smoking and cartilage loss include:

Smoking may disorder the cells and deter cell production in cartilage.

Smoking may raise levels of toxins in the blood, contributing to cartilage loss.

Smoking may increase carbon monoxide levels in the blood, affecting blood oxygenation, which could impede cartilage repair.

The smokers also had higher pain scores than the non-smokers.

Since cartilage does not have pain fibers, increased pain may not be caused by cartilage loss. However, smoking may impact other structures in the knee or may have an effect on pain perception.

Smoking Protects Against Knee Osteoarthritis

According to the September 2007 issue of Osteoarthritis and Cartilage, researchers analyzed the connection between x-ray evidence of knee osteoarthritis and obesity and occupation.

Unexpectedly, during that analysis, researchers found a modest protective effect of smoking on the development of osteoarthritis.

To confirm the findings, researchers also analyzed data from the Framingham Osteoarthritis Study and found that smokers had a lower rate of osteoarthritis than non-smokers. The effect of nicotine on the chondrocytes (a layer of cells) in articular cartilage may account for the protective effect.

Similarly, in an older study published in February 1989 in Arthritis & Rheumatism, while studying knee osteoarthritis in the first Health and Nutrition Examination Survey, researchers unexpectedly found a protective association between smoking and osteoarthritis after adjusting for age, sex, and weight.

Based on their own findings and the comparison with the Framingham Osteoarthritis Study, researchers concluded that smoking or some unknown or unidentified factor related to smoking modestly protects against the development of knee osteoarthritis.

The Chingford Study: Smoking and Risk of Osteoarthritis in Women

A study, published in the February 1993 Annals of the Rheumatic Diseases, looked at cigarette smoking and the risk of osteoarthritis in women in the general population.

Since previous studies concluded that smoking had a protective effect against the development of knee osteoarthritis, 1,003 women from the Chingford (greater London, England) general population were studied. There were 463 women classified as ever smokers (consumed an average of 14.9 cigarettes a day for a mean of 25.7 years) and 540 non-smokers. Hand and knee x-rays were used to assess osteoarthritis. Results did not support an inverse association between smoking and osteoarthritis in women. Inverse association would mean as smoking increased, osteoarthritis decreased -- and this theory was not supported by the Chingford study.

The Clearwater Osteoarthritis Study

Yet one more study, known as the Clearwater Osteoarthritis Study, published in the January 2003 Osteoarthritis and Cartilage concluded that smoking did not appear to significantly protect against the development of osteoarthritis. The conclusion followed examination of 2505 men and women. The study participants were examined for osteoarthritis at 4 sites -- knee, hand, foot and cervical spine. Self-reported history of smoking determined smoking status.

Conclusion About Smoking and Osteoarthritis

With the well-known health hazards related to nicotine, it would be impossible to recommend smoking, even if more studies pointed to a protective effect on osteoarthritis. Researchers are far from concluding that there is any substantial benefit associated with smoking.

Sources:

Cigarette smoking and the risk of cartilage loss and knee pain in men with knee osteoarthritis. Annals of the Rheumatic Diseases. S Amin et al. January 2007.

Smoking and osteoarthritis: Is there an association? The Clearwater Osteoarthritis Study. Osteoarthritis and Cartilage. Wilder FW et al. January 2003.

Does smoking protect against osteoarthritis? Arthritis & Rheumatism. Felson MD, David T. et al. February 1989.

Cigarette smoking and risk of osteoarthritis in women in the general population: the Chingford study. Hart, DJ and Spector, TD. Annals of the Rheumatic Diseases. February 1993.

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By (user no longer on site)
over a year ago


"it appears smoking is good for people who suffer specifically with osteoarthritis, although overall smoking is considered bad for your health.

.

A causal inverse relationship between smoking and osteoarthritis (OA) has been suggested by several retrospective studies. Data from the Clearwater OA review suggest that smokers demonstrate significant levels of protection from OA at four (knee, hand, foot and spine) sites1. Smoking decreases the risk of developing OA in overweight individuals2 and a negative correlation is found between smoking and large joint OA3. In the Chingford study4, a non-significant albeit 40% reduction of radiological OA was seen in smokers. Finally, modest protection against development of knee OA was found by Felson et al.5. Of the more than 400 agents found in cigarette smoke, nicotine is one of the most physiologically active components. An in vitro study recently published demonstrates that nicotine is a potent stimulator of bone cell synthetic activity while a condensate of cigarette smoke was markedly inhibitory6. It was suggested that components of smoke, other than nicotine, were responsible for the adverse skeletal effects. To ascertain whether a similar phenomenon existed in articular cartilage we examined the dose-dependent direct effect of nicotine on human articular chondrocytes. Since articular cartilage is without a vascular supply, it is reasonable to expect that the chondrocyte response would reflect the in vivo situation and mimic the direct effect of circulating levels of nicotine on articular chondrocytes

.

Chondrocytes isolated by trypsin digestion from a normal human femoral head were grown to confluency in F-12 media containing 10% fetal calf serum, 50 µg/ml ascorbic acid and antibiotics. Experiments were initiated by dispersing 25,000 cells/cm2 into individual wells of 12-well culture plates. When the secondary cultures reached confluency they were exposed to varying dosages of nicotine (2.5, 12.5, 25, 50 and 250 ng/ml) which bracketed the average 25 ng/ml seen in smokers consuming one pack of cigarettes/day7. A minimum of six replicates were used in duplicate experiments with exposure limited to 72 h. Four hours prior to termination, 10 µCi/ml each of tritiated proline and 35-sulfate were added for analysis of collagen and glycosaminoglycan (GAG), respectively.

Isotope incorporation into the cell layer was assayed following thorough washing and high speed homogenization. Aliquots were removed for assay of DNA and sulfated GAG with 1,9-dimethylmethylene blue following 0.4% pronase/papain digestion. Uptake of labeled sulfate was assayed by liquid scintillation counting in the dual label mode while collagen analysis followed 6 N HCl hydrolysis and separation of labeled proline from hydroxyproline by silica gel G thin layer chromatography. Identity of the imino acids was based on comparison with authentic standards. The data reported as the mean±S.E.M. of the specific activity of GAG (counts per minute (CPM) 35SO4/µg GAG) and specific activity of collagen (CPM Hyp/µg Hyp) were statistically analyzed using the student's t test and ANOVA.

Based on these observations, we can only confirm that nicotine at physiological levels found in average smokers is a potent stimulator of protein, including collagen, synthesis in chondrocytes as well as bone cells. Nicotine, at physiological levels found in smokers, increases DNA, GAGs and collagen synthesis of nucleus pulposus cells10 but at higher levels was inhibitory. A second study on similar cell cultures noted significant depression of GAG and collagen synthesis albeit at pharmacological nicotine levels of 100 µg/ml and an exposure period of 7 days11. The metabolic assays performed are rate oriented (specific activity) insofar as they measure the amount of synthesis in the time interval of isotope exposure. No attempt was made to differentiate the types of collagen or proteoglycan synthesized. Based on our data, the often alluded to “protective” effect of smoking in OA may have as its basis an alteration in metabolism of chondrocytes

"

Too much spare time and google right there.

I suspect most people who smoke, know the dangers.

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By *opsy RogersWoman
over a year ago

London

...and let's not get osteoarthritis confused with rheumatoid or juvenile arthritis.

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By *ce WingerMan
over a year ago

P.O. Box DE1 0NQ

I've only got psioratic arthritis, so I'm out

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By (user no longer on site)
over a year ago


"Is the benefit of smoking worth the risks of lung cancer or any other smoking related diseases?

Probably not."

Actually i mean definetly not. I'm not about to start smoking !

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