The patient’s medical history was significant for hypertension. Current medications included hydrochlorothiazide 25 mg and atenolol 25 mg.
Review of Systems
- Vital signs
- Blood pressure: 134/72 mmHg
- Pulse: 69 beats/min
- Respiration: 12 breaths/min
The patient reports that he has not seen a dentist in over 25 years. Previous active dental treatment had involved extractions and fabrication of maxillary right and mandibular left fixed bridges. The patient reports that he brushes once a day and has never flossed.
The patient has smoked a pack of cigarettes a day since he was 11 years old (48 pack years). He does not drink alcohol.
Extraoral and Intraoral Examination
There were no significant extraoral findings, no swellings, or masses detected. Intraoral examination revealed generalized poor oral hygiene and a very strong scent of tobacco on breath. The gingiva was generally fibrotic with minimal bleeding upon probing. Periodontal probing depths ranged from 5 to 12 mm, with generalized advanced furcation defects on all molar teeth. Unopposed tooth #16 was extruded and grossly carious (see Figure 5.1.1).
Generalized severe chronic periodontitis (Armitage 1999).
The initial treatment plan for the patient included smoking cessation counseling, home care education, and extraction of teeth #1, #3, #14, #16, #18, #29, and #30. Postoperative pain was effectively managed with a combination of 400 mg ibuprofen and 500 mg acetaminophen every six hours. Following scaling and root planing therapy, transitional removable partial dentures were fabricated.
The relief of oral pain is one of the primary obligations of a dental professional. Dental diseases and the treatment of dental diseases both have the potential to cause pain. Most dental pain has an inflammatory component. The most effective analgesics used for dental pain have anti‐inflammatory properties (see Table 5.1.1).
Table 5.1.1: Commonly used systemic analgesics.
|Aspirin||Bayer||325–650 mg Q6H||Antiplatelet effect
Aggravation of asthma
Interaction with warfarin
|Ibuprofen||Motrin||200–600 mg Q6H||Antiplatelet effect
Aggravation of asthma
Altered kidney function
|Naproxen sodium||Aleve||220–550 mg Q8H||Antiplatelet effect
Aggravation of asthma
Altered kidney function
|Diflunisal||Dolobid||500 mg Q12H||Antiplatelet effect
Interaction with warfarin
Aggravation of asthma
|Acetaminophen||Tylenol||325–650 mg Q6H||Liver toxicity||OTC|
Nonsteroidal anti‐inflammatory drugs (NSAIDs) are the most common agents used to relieve oral pain, with both prescription (Rx) and over the counter (OTC) products available. NSAIDs have analgesic, anti‐inflammatory, antipyretic, and antiplatelet properties (see Table 5.1.2). The principle mechanism of action of NSAIDs is the competitive, reversible inhibition of the conversion of arachidonic acid to prostaglandins by cyclooxygenase (COX) enzymes. There are two isoforms of COX enzymes, COX‐1, and COX‐2. Arachidonic acid is converted to thromboxane A2 by the COX‐1 enzyme, leading to platelet aggregation. Arachidonic acid is converted to prostaglandins by the enzyme COX‐2, leading to inflammation and pain. There are several NSAID products, each with subtle differences in their abilities to block COX‐1 and COX‐2. These differences account for the products variability in potency, dosing, adverse drug reactions, and clinical therapeutic indications. NSAIDs, as a class, are known as having the side effects of gastrointestinal (GI) bleeding, altered renal (kidney) effects, an aggravation of asthma in susceptible individuals, and antiplatelet effects that may cause postoperative bleeding. Newer NSAIDs have been developed that are selective COX‐2 inhibitors; however they have been implicated as having increased risk of cardiovascular events (Laskarides 2016).
Table 5.1.2: Effects of cyclooxygenase inhibition by aspirin and NSAIDs (“4 A’s of NSAIDs”).
NSAIDs have the potential of drug interactions due to their effects on the COX enzymes (see Table 5.1.3). NSAIDs may decrease the hypotensive effects of certain antihypertensive medications (beta‐blockers, angiotension converting enzyme inhibitors, and diuretics). NSAIDs may increase the hypoglycemic effects of the sulfonylurea class of oral antidiabetic agents. NSAIDs may also increase the blood levels of the psychiatric medication lithium, leading to potential lithium toxicity.
Table 5.1.3: Potential drug interactions due to cyclooxygenase inhibition and prostaglandin reduction.
|Decreased effectiveness of both thiazide and loop diuretics (used for hypertension)|
|Decreased effectiveness of beta‐blockers (used for hypertension)|
|Decreased effectiveness of angiotension converting enzymes inhibitors (used for hypertension)|
|Increased effectiveness of sulfonylureas (used for diabetes)|
|Increased blood levels and toxicity of lithium (used for bipolar disorder)|
The most commonly used NSAIDs are ibuprofen and naproxen sodium. Ibuprofen is available in both OTC and RX formulations, with common dosing of 200–600 mg every six hours. Naproxen sodium is available in both OTC and RX formulations with common dosing of 220–550 mg every eight hours.
Aspirin is a salicylate nonnarcotic analgesic with analgesic, anti‐inflammatory, antipyretic, and antiplatelet properties. Aspirin irreversibly blocks both COX‐1 and COX‐2 and is known as having greater antiplatelet activity than NSAIDs. Low‐dose aspirin (81 mg per day) is frequently recommended by physicians for prevention of stroke or heart attack due to its antiplatelet properties. The usual analgesic dose of aspirin is 325–650 mg every six hours. The prescription drug diflunisal is a salicylate used at a dose of 500 mg every 12 hours. In addition to the common side effects of GI bleeding, aggravation of asthma, altered renal function, and antiplatelet effects, salicylates have the unique side effects of vertigo, tinnitus, and ototoxicity. The risk of ototoxicity is increased when salicylates are used along with other ototoxic medications such as loop diuretics (Weinberg et al. 2013).
Salicylates share the same potential for drug side effects as other cyclooxygenase blocking agents. Salicylates have the side effect of displacing the anti‐Vitamin K blood thinner warfarin from its plasma protein binding sites, increasing therapeutic blood levels of active warfarin. Aspirin should be used with great caution in patients taking therapeutic levels of warfarin due to a significant risk of postoperative bleeding related to both the increased blood levels warfarin and the antiplatelet actions of aspirin (see Table 5.1.4).
Table 5.1.4: Special patient populations that may complicate the choice of an analgesic.
|Peptic ulcer disease||Aspirin and NSAIDs may cause GI bleeding|
|Alcoholism||Aspirin and NSAIDs may cause GI bleeding. Acetaminophen is hepatoxic|
|Kidney disease||NSAIDs may alter kidney function|
|Patient on warfarin||Aspirin may reduce protein binding of warfarin. Aspirin and NSAIDs have antiplatelet effects|
|Hypertension||NSAIDs may reduce efficacy of antihypertensives|
|Diabetes||NSAIDs may increase efficacy of sulfonylureas|
|Arthritis||Patient may be taking other OTC or RX NSAIDs|
Acetaminophen is a drug that does not fall into a specific category. It is not a salicylate; it is not an NSAID; it does not block COX. The exact mechanism of action of acetaminophen is not known. Theories of its action include a possible inactivation of COX enzymes, inhibition of nitric acid production, or blockade of prostaglandin (Guggenheimer and Moore 2011; Moore and Hersh 2013; Laskarides 2016). Acetaminophen has analgesic and antipyretic properties, but does not have anti‐inflammatory or antiplatelet properties. Its acute pain relief properties are less than that achieved by NSAIDs. Acetaminophen is commonly dosed at 325–650 mg every six hours, with occasional dosing of 1000 mg every six hours. It is generally considered safe for most patients, including children and pregnant women, when used as directed. Unlike salicylates or NSAIDs, it is not associated with GI bleeding and does not inhibit platelet aggregation. Acetaminophen is hepatotoxic, causing severe liver damage (possibly fatal) when used at excessive dosage, when used along with other hepatoxic drugs, or when used by individuals who consume three or more alcoholic beverages daily (Guggenheimer and Moore 2011). The maximum daily dose of acetaminophen as recommended by the US Food and Drug Administration (FDA) is 4000 mg per day. Recently, a leading drug manufacturer of acetaminophen changed its packaging instructions to reflect a maximum daily dose of 3000 mg per day due to concerns over liver toxicity (Moore and Hersh 2013).
The risk of a patient taking an inappropriate dose of acetaminophen and suffering a hepatic event is complicated by the fact that multiple OTC products containing acetaminophen are marketed for a variety of symptoms (cough and cold products, migraine pain products, arthritis pain products, etc.). The inclusion of acetaminophen as an ingredient is frequently listed in small print on the back the product packaging. Many patients do not read ingredient labeling and assume that the product is safe because it is available OTC. Patients may be unaware of the potential of duplicating medication if they take acetaminophen for relief of dental pain (see Table 5.1.5). The prudent clinician regularly asks his patients about all medications (RX and OTC) they are taking in an attempt to avoid inappropriate use.
Table 5.1.5: OTC products that may contain acetaminophen.
|Cough and cold products|
|Cold and flu products|
|Migraine relief products|
|Arthritis pain relief products|
|Menstrual cramp relief products|
|Back pain relief product|
Combination analgesic therapy is frequently used in the management of postoperative oral pain. The use of ibuprofen at a dose of 200–600 mg combined with acetaminophen at a dose of 500–1000 mg every six hours has been evaluated in multiple pain studies. The combination has been shown to provide pain relief that is superior to that provided by either product alone and at lower doses (Ong et al. 2010; Moore and Hersh 2013). Ibuprofen‐acetaminophen combination therapy has also been demonstrated to provide pain relief comparable to that provided by common acetaminophen‐opioid combinations (acetaminophen and codeine, acetaminophen and hydrocodone, acetaminophen and oxycodone) for moderate to severe pain without the inherent risks of opioid therapy (Ong et al. 2010; Moore and Hersh 2013).
- Acetaminophen is not known to be a teratogen and is generally considered safe for use during pregnancy when used as directed. Acetaminophen is not a narcotic and does not contribute to narcotic (opioid) addiction. Acetaminophen is a known hepatotoxin and may cause severe liver damage. This risk is greatly increased in individuals who consume three or more alcoholic beverages a day or use other medications that are hepatoxic. The salicylate class of medications (such as aspirin) is known to cause tinnitus.
- The combination of an NSAID with acetaminophen provides superior relief of pain at lower dosages than that provided by either product alone. The reason for this is not known, as the mechanism of action of acetaminophen is unknown. While NSAIDs act by competing with arachidonic acid and blocking the actions of the cyclooxygenase enzymes, acetaminophen may function by inactivating the cyclooxygenase enzymes themselves. The combination of an NSAID and acetaminophen provides comparable pain relief to that achieved by a combination of acetaminophen with an opioid narcotic, while avoiding the adverse effects of sedation and impaired functioning.
- Atrial fibrillation is a type of cardiac arrhythmia. Cardiac stents are utilized in the management of coronary artery disease. Both atrial fibrillation and coronary artery disease are treated with blood thinners. Warfarin is an anti‐Vitamin K anticoagulant that alters the clotting cascade. Warfarin is a highly protein‐bound medication. Nonprotein bound warfarin inhibits the synthesis of Vitamin K dependent clotting factors II, VII, IX, and X. Aspirin displaces warfarin from protein binding sites, increasing the levels of active free warfarin. Active free warfarin increases potential for bleeding. Clopidogrel is an antiplatelet agent. It inhibits platelet aggregation, as does aspirin and naproxen sodium. The combination increases the potential for bleeding. Acetaminophen does not have antiplatelet activity and it is not highly bound to plasma protein.