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An Orthopedic Pain Med for Dental Implantologists

For pain control in dentistry, we deal with pain from periodontal therapy, endodontic therapy, and implant therapy. These surgeries deal with different tissues and these tissues are likely to respond differently to different pain medications. However, orthopedic surgeons and dental implantologists both work primarily with bone, and we can benefit from sharing information on the types of pain meds that best benefit our patients after skeletal surgery. One pain medication that is popular with orthopedic surgeons but is seldom used by implantologists is diclofenac. First synthesized in 1973, diclofenac is the most prescribed NSAID worldwide. The brand name of this medication is Voltarin, and is commonly used as a topical pain medication that is applied as a cream. Diclofenac is considered a type of NSAID and carries with it all of the potential side effects of the NSAIDs. In the following chart, diclofenac is listed to inhibit bone resorption.

Diclofenac is a nonsteroidal anti-inflammatory drug (NSAID) that is commonly used to control pain and reduce inflammation. It works by inhibiting the activity of an enzyme called cyclooxygenase (COX). There are two main isoforms of this enzyme, COX-1 and COX-2.

  • Inhibition of COX-2: Diclofenac primarily inhibits the activity of cyclooxygenase-2 (COX-2), an enzyme that is responsible for the synthesis of prostaglandins. Prostaglandins are chemical messengers in the body that promote inflammation, pain, and fever. By inhibiting COX-2, diclofenac reduces the production of prostaglandins, thereby decreasing inflammation and alleviating pain.
  • Inhibition of COX-1: Diclofenac also inhibits COX-1, although to a lesser extent than COX-2. COX-1 is an enzyme that plays a role in the production of prostaglandins involved in normal physiological processes, such as protecting the stomach lining. The inhibition of COX-1 can contribute to the side effects of NSAIDs, including gastrointestinal irritation and ulceration.

Diclofenac primarily exerts its anti-inflammatory and analgesic effects through the inhibition of cyclooxygenase (COX) enzymes, particularly COX-2. While diclofenac is not specifically known for directly inhibiting bone resorption, its anti-inflammatory actions may indirectly influence the bone resorption process.

Bone resorption is a complex physiological process involving the breakdown of bone tissue by osteoclasts. Prostaglandins, which are lipid compounds derived from arachidonic acid, play a role in regulating osteoclast activity.

By inhibiting COX-2 and reducing the production of prostaglandins, diclofenac may indirectly affect osteoclast function. Prostaglandins are known to stimulate osteoclast activity, and their reduction may lead to a decrease in bone resorption. However, the relationship between NSAIDs like diclofenac and bone metabolism is complex, and the effects on bone can vary depending on factors such as dosage, duration of use, and the specific conditions being treated.

While inhibiting bone resorption sounds like a good feature from a bone regeneration and dental implantology standpoint, we need to recognize that part of all regenerative procedures involve trauma to the tissues which require an acute inflammatory response to clear damaged tissues before regeneration can occur. Before integration to our implants can occur, damaged bone must be cleared via an acute inflammatory response prior to bone formation on the implant surface. Prostaglandins are involved in the early stages of acute inflammation. They are lipid compounds derived from arachidonic acid and are produced in response to tissue injury or infection. In acute inflammation, prostaglandins contribute to the dilation of blood vessels (vasodilation), increased permeability of blood vessels (resulting in edema), and the recruitment of immune cells to the site of injury or infection. These actions help to initiate the inflammatory response and promote the clearance of damaged cells.

So let’s think this through.

We have a pain med that inhibits the acute inflammation that is needed to remove the damaged tissue that lines the osteotomy before bone can be formed on the implant surface, but the medication does not inhibit bone formation. The medication is only prescribed for 7 days and often is not taken for the full time period. When the time frame for effective integration is considered to be in the rage of 4 to 12 weeks, depending on the vitality of the bone, our assessment is that a slight delay in integration by reducing the inflammatory response has no effect on the success of implant integration. In our clinic, where we follow bone regeneration and implant integration closely, we have seen no negative effects of diclofenac on implant integration.

We have been using diclofenac as our primary post-surgical pain medication for over a year, and while we have had no reported side effects to the medication, it has been a game changer for pain control. While we have not instituted any formal evaluation of the effectiveness of diclofenac to control post operative pain in our patients, what we have noticed is a significant reduction in patients complaining of post operative pain. In our experience, we have found diclofenac to be superior to Tramadol and Norco for for both pain control and side effects.

For those interested: Diclofenac potassium 50 mg TID

For more detailed information on diclofenac:

For a greater understanding of bone resorption and regeneration please view this free CE course:

Short Course on Bone Science (2 CE)

MEMBER:

American Society for Bone and Mineral Research (ASBMR)

Tissue Engineering and Regenerative Medicine International Society (TERMIS)

American Academy of Implant Dentistry (AAID)

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