If you take painkillers for osteoarthritis, you should be careful about the disease progression?

*For reference only for medical professionals, can I take painkillers? Osteoarthritis (OA) is a chronic disease characterized by inflammation, cartilage loss and bone remodeling.
It is the main cause of disability and reduced quality of life.

The knee joint is often affected, and approximately one-third of adults over the age of 45 have knee OA (KOA).

X-ray is essential for diagnosing OA! X-ray examination is the "gold standard" for diagnosing osteoarthritis.

The three typical manifestations of OA on X-ray films are: asymmetrical joint space narrowing of the affected joint, subchondral bone sclerosis and/or cystic degeneration, and osteophyte formation on the joint edges.

Some patients may have different degrees of joint swelling, free bodies can be seen in the joints, and even joint deformation [1-2].

The diagnosis of OA can be seen in Table 1.

Table 1 Recommendations for the diagnostic criteria of KOA, and the six major drug treatments in the OA management guidelines recommend drug treatments as follows: 1.
Non-steroidal anti-inflammatory drugs (NSAIDs): are the most commonly used drugs for OA patients to relieve pain and improve joint function.

Including topical drugs and systemic drugs.

2.
Analgesics: Those who are ineffective or intolerant to NSAIDs can use non-NSAIDs, opioid analgesics, and a combination of acetaminophen and opioids.

3.
Injection of drugs into the joint cavity: It can effectively relieve pain and improve joint function.

However, this method is an invasive treatment, which may increase the risk of infection.
It must be strictly aseptic and standardized.

(1) Glucocorticoid: It has a rapid onset of action and has a significant short-term pain relief effect.
However, repeated application of hormones will have adverse effects on articular cartilage.
It is recommended to use no more than 2 to 3 times per year, and the injection interval should not be shorter than 3 -6 months. (2) Sodium hyaluronate: It can improve joint function, but its role in cartilage protection and delaying the disease process is still controversial.
It is recommended to use it according to the patient's individual situation.

(3) Medical chitosan: It can promote the synthesis of extracellular matrix of cartilage cells, reduce inflammation, and regulate cartilage cell metabolism; it has viscoelasticity, slow absorption, and can be used as a supplementary component of synovial fluid, slowing down the progression of arthritis and reducing joint pain , Improve function, suitable for early and middle OA patients, 2-3 injections per course of treatment, 1-2 courses per year.

(4) Growth factors and platelet-rich plasma: can improve local inflammation, and can participate in the repair and regeneration of intra-articular tissue; however, further research is needed for its mechanism and long-term efficacy.
Clinically, patients with symptomatic OA can choose Sexual use.

4.
Slow-acting drugs (SYSADOAs) to relieve OA symptoms: including diacerein, glucosamine, etc.

5.
Anti-anxiety drugs: It can be applied to OA patients with long-term persistent pain, especially patients who are not sensitive to NSAIDs drugs, and can achieve the purpose of alleviating pain and improving joint function in a short time.

6.
Chinese patent medicines: including oral Chinese patent medicines and topical plasters containing artificial tiger bone powder, Jintiesuo and other effective ingredients.

Is osteoarthritis worsened after using NSAIDs? However, the long-term effects of these drugs on structural progression are unclear.

The structural progression of KOA is related to the gradual deterioration of pain symptoms [3-5].

Most guidelines recommend the use of analgesics as a first-line intervention after core treatment.

NSAIDs and cyclooxygenase-2 (COX-2) inhibitors are the most commonly used analgesics.

The effect of analgesia on the structure of KOA is unclear.

A few in vitro studies have shown that some NSAIDs may inhibit the synthesis of cartilage matrix, thereby promoting the development of OA.

A recent study [6] found that in KOA patients, compared with patients who did not use NSAIDs, patients treated with NSAIDs decreased the minimum joint space width (mJSW) on the medial knee joint, which led to the progression of osteoarthritis.

Figure 1 Screenshot of the study.
The study is a multicenter, observational cohort study involving 4796 KOA patients, excluding participants with inflammatory arthritis, including rheumatoid arthritis (RA), gout, or psoriatic arthritis (PsA), and history of knee-related injuries and/or surgery.

At baseline, 12, 24, 36, 48, 72, and 96 months of follow-up, each year, the bilateral anterior flexion knee fixation films were obtained.

The mJSW of the medial knee joint was measured.
X-rays were used to score OA using the Kellgren-Lawrence (KL) grading standard.
KL≥2 indicates the presence of KOA.

The study investigated the drugs used by KOA patients in 8 years.
There are 7 kinds of drugs, namely NSAIDs (14.
7%), antihistamines (10.
4%), statins (27.
4%), antihypertensive drugs (15.
0%), Antidepressant, anxiety, psychotropic drugs (14.
0%), osteoporosis-related drugs (10.
9%) and diabetes-related drugs (6.
9%).

Among the 7 specific drug categories, compared with patients who are not currently using NSAIDs, the mJSW of patients using NSAIDs decreased by 0.
042mm (β=0.
042, 95%CI 0.
08-0.
0004, P=0.
048).

For other analgesics, no significant association was observed, including acetaminophen (β=-0.
043, 95% CI -0.
12~0.
03, P=0.
25), COX-2 inhibitors (β=-0.
046, 95% CI -0.
13~0.
035, P=0.
27) and corticosteroids (β=-0.
006, 95%CI -0.
06~0.
04, P=0.
81). Other types of drugs did not show any association, including osteoporosis drugs (β=0.
01, 95%CI -0.
05~0.
07, P=0.
75), statins (β=-0.
034, 95%CI -0.
08~ 0.
01, P=0.
11), antihistamines (β=0.
03, 95%CI -0.
03~0.
09, P=0.
30), antidepressants (β=-0.
048, 95%CI -0.
10~0.
01, P=0.
095) And diabetes drugs (β=-0.
02, 95% CI -0.
05~0.
1, P=0.
56).

In addition, no association was observed with cardiovascular drugs, including β blockers (β=-0.
02, 95% CI -0.
07~0.
03, P=0.
38), angiotensin converting enzyme inhibitors (β=-0.
015, 95% CI -0.
06~0.
03, P=0.
53), angiotensin receptor blockers (β=0.
026, 95% CI -0.
03~0.
08, P=0.
35) and calcium channel blockers (β=-0.
04, 95% CI -0.
09~0.
01, P=0.
11) (see Table 2).

Table 2 The effect of the relationship between mJSW and drug use is estimated.
This is strange.
NSAIDs, as the first-line drugs for the treatment of OA, actually lead to the progression of OA disease! Why? A study by Driban et al.
[7] found that KOA patients who insisted on using NSAIDs for 36 months had a reduction in the width of the medial joint space (JSW) on both left and right knee joints compared with those without NSAIDs.

Another study [8] found that over a period of 4 years, patients who used NSAIDs frequently (compared with patients who used it less frequently) had a decrease in JSW, although this relationship was not statistically significant.

However, this study surpassed these studies and examined the relationship between current use of NSAIDs and changes in mJSW during a 96-month follow-up.

Evidence from in vivo and in vitro studies indicates that specific NSAIDs may inhibit matrix proteoglycan [10] synthesis by acting on enzymes involved in the biosynthesis of chondroitin sulfate [9], leading to increased vulnerability of chondrocytes and cartilage degeneration.

However, the results still need further research to confirm these findings with clinical trial data.

Therefore, patients with OA still need to take the medicine according to the doctor's recommendation, and must not stop the medicine by themselves.