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Dovlatova N, Jakubowski J, Sugidachi A, Heptinstall S. The reversible P2Y12 antagonist cangrelor influences the ability of the active metabolites of clopidogrel and prasugrel to produce irreversible inhibition of platelet function. J Thrombosis Haemost. 2008; 6:1153-1159
Lillis T, Ziakas A, Koskinas K Safety of dental extractions during uninterrupted single or dual antiplatelet treatment. Am J Cardiol. 2011; 108:964-967 https://doi.org/10.1016/j.amjcard.2011.05.029
Dinkova AS, Atanasov DT, Vladimirova-Kitova LG. Discontinuation of oral antiplatelet agents before dental extraction – necessity or myth?. Folia Med (Plovdiv). 2017; 59:336-343
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Pirmohamed M. Warfarin: almost 60 years old and still causing problems. Br J Clin Pharmacol. 2006; 62:509-511
Hirsh J, Fuster V, Ansell J, Halperin JL. American Heart Association/American College of Cardiology foundation guide to warfarin therapy. J Am Coll Cardiol. 2003; 41:1633-1652
Coons J, Empey P. Drug metabolism in cardiovascular disease. In: Xie W (ed). San Diego, CA, USA: Elsevier; 2016
Abdullah WA, Khalil H. Dental extraction in patients on warfarin treatment. Clin Cosmet Investig Dent. 2014; 6:65-69 https://doi.org/10.2147/CCIDE.S68641
Costantinides F, Rizzo R, Pascazio L, Maglione M. Managing patients taking novel oral anticoagulants (NOAs) in dentistry: a discussion paper on clinical implications. BMC Oral Health. 2016; 16 https://doi.org/10.1186/s12903-016-0170-7
Romond KK, Miller CS, Henry RG. Dental management considerations for a patient taking dabigatran etexilate: a case report. Oral Surg Oral Med Oral Pathol Oral Radiol. 2013; 116:e191-195 https://doi.org/10.1016/j.oooo.2013.05.001
Mingarro-de-Leon A, Chaveli-Lopez B. Alternative to oral dicoumarin anticoagulants: considerations in dental care. J Clin Exp Dent. 2013; 5:e273-278 https://doi.org/10.4317/jced.51226
Tran A, Cheng-Lai A. Dabigatran etexilate: the first oral anticoagulant available in the United States since warfarin. Cardiol Rev. 2011; 19:154-161
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Connolly SJ, Ezekowitz MD, Yusuf S Dabigatran versus warfarin in patients with atrial fibrillation. N Engl J Med. 2009; 361:1139-1151 https://doi.org/10.1056/NEJMoa0905561
Eikelboom JW, Wallentin L, Connolly SJ Risk of bleeding with 2 doses of dabigatran compared with warfarin in older and younger patients with atrial fibrillation: an analysis of the randomized evaluation of long-term anticoagulant therapy (RE-LY) trial. Circulation. 2011; 123:2363-2372 https://doi.org/10.1161/CIRCULATIONAHA.110.004747
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The impact of drug therapy on minor oral surgery procedures Khadeeja Saleem Paras Ahmad Jawaad Ahmed Asif Mohmed Isaqali Karobari Tahir Yusuf Noorani Dental Update 2024 48:11, 707-709.
Authors
KhadeejaSaleem
BDS, MSc
Postgraduate student, Oral Medicine Unit; School of Dental Sciences, Universiti Sains Malaysia
Senior Lecturer, Conservative Dentistry Unit, School of Dental Sciences, Universiti Sains Malaysia, Health Campus, 16150 Kubang Kerian, Kota Bharu, Kelantan, Malaysia.
Some advanced and slightly more invasive treatments require the use of certain drugs before, during and after the treatment like local anesthetics, vasoconstrictors, anxiolytics, analgesics and antibiotics. All of these can possibly interact with medications a patient is already taking and can also interfere with the current dental treatment and create complications. This article aims to provide necessary information about commonly encountered systemic diseases and associated treating medications, their mechanism of action, possible complications and their management.
CPD/Clinical Relevance: This article discusses drugs that are used for treating various systemic conditions, but can have a harmful effect on minor oral surgery procedures.
Article
Minor oral surgical procedures are performed daily around the globe. These forms of minor oral surgery are not restricted to just removing impacted teeth or severely broken-down teeth, they also include apicectomy, biopsy, placement of dental implants, sinus lift and other procedures. These procedures impose a substantial risk of bleeding, dry socket, infection and bone necrosis. Every patient is at risk of developing a complication; however, the risk is increased in patients being treated for various systemic diseases. Table 1 describes the risk of common complications during or after dental procedures.
Category
Drug
Commercial names
Mechanism of action
Dental considerations
Management
Anti-platelet drugs
Aspirin
Micropirin, Nu seals, Danamep
Anti-platelet
Excessive bleeding, delayed healing
INR testNo alteration in dose is required.Perform the procedure as minimally invasively as possible, use of local haemostatic measures
DMARD: disease-modifying anti-rheumatic drugs; INR: international normalized ratio; MRONJ: medication-related osteonecrosis of the jaw; TT: thrombin time; PTT: partial thromboplastin time
This article gathers and analyses those drugs that are used for treating various systemic conditions, but can have a deleterious effect on minor oral surgery. Although these drugs are not prescribed by dentists, dentists will certainly encounter patients using a spectrum of drugs that are often novel, and post-dental treatment complications and management in such patients should be known to every dentist.
There are many drugs that have been developed that GDPs should be aware of. General dentists and oral surgeons are continually advised about the importance of obtaining a thorough history from patients about past and common systemic diseases and their medicinal management to prevent any complications, mild or severe.
This article provides information about commonly encountered systemic diseases and the associated drug treatments, their mechanism of action, possible complications and management. The classes of drugs discussed include anti-platelet agents, vitamin K antagonists, novel oral anticoagulants, bisphosphonates and disease-modifying anti-rheumatic drugs.
Anti-platelet drugs
As the name suggests, these medications have been used to inhibit platelet aggregation/agglutination to prevent clot formation, especially in individuals with compromised cardiovascular systems, coronary artery thrombosis, stroke and deep vein thrombosis. Although aspirin has been used for inhibition of platelet aggregation for decades, new medications with better efficacy have flooded the market. Currently, the anti-platelet medications being prescribed are acetylsalicylic acid (ASA) or aspirin (Asaphen, Entrophen, Novasen), clopidogrel (Plavix), prasugrel (Effient), ticagrelor (Brilinta), cangrelor, eptifibatide, tirofiban, cilostazol (Pletal), and dipyridamole (Persantine). Table 2 describes the risk of procedures with regard to the type of anti-thrombotic agent being used.
Anti-platelets
Vitamin K antagonists
Novel anticoagulants
Low-risk procedures
No change
No change
No change
Medium-risk procedures
No changeLocal haemostatic measures
For INR ≤4, no changeLocal haemostatic measures
No changeLocal haemostatic measures
High-risk procedures
No changeLocal haemostatic measures
For INR ≤3, no changeFor INR ≥3, consider:Low risk of thrombo-embolismWithdrawal of drugf or reduce dose to allow INR to fallHigh risk of thrombo-embolism:Withhold warfarin, convert to LMWH and withhold LMWH on the morning of the procedure
Withhold 24 hours prior to the procedureLocal haemostatic measuresRestart after haemostasis is achieved
INR: international normalized ratio; LMWH: low-molecular-weight heparin.
Platelet aggregation is reversed and/or prevented by anti-platelet drugs in arterial thrombosis. This is most prominently seen in ischaemic stroke and myocardial infarction. Haemostatic plugs form when platelets aggregate at the site of vascular injury.
Aspirin
The name, Aspirin, for acetylsalicylic acid (ASA) was coined by Bayer in 1899. Aspirin entered the Guinness World Records for being the most sold painkiller in 1950. It was one of the first drugs to come into common usage. Aspirin remains one of the most researched medicines in the world, with approximately 700 to 1000 clinical trials conducted each year.1
Mechanism of action of ASA (Aspirin, Asaphen, Entrophen, Novasen)
Acts on the arachidonic acid pathway where the acetyl groups of ASA bind with a serine residue of the cyclo-oxygenase-1 (COX-1) enzyme and inhibit the production of prostaglandins and thromboxane A2 (TXA2), which subsequently inhibits the platelet aggregation.
Eptifibatide and tirofiban act as antagonists of fibrinogen binding to the GP IIb/IIIa receptor (surface receptor) and thus inhibit platelet aggregation.
Enzyme inhibitors
Cilostazol (Pletal) and dipyridamole (Persantine) inhibit both adenosine deaminase and phosphodiesterase in platelets, and lead to elevation of intra-platelet cyclic AMP, which reduces thromboxane A2 activity, leading to inhibition of platelet aggregation.
Dental considerations
The guidelines presented by the British Committee for Standards in Haematology2 state the following:
The risk of bleeding with a stable international normalized ratio (INR) that lies within the therapeutic range (<4) is minimal.
The risk of thrombosis may increase in patients if the oral anticoagulants are temporarily stopped.
If INR in patients is unstable, the relevant physician should be consulted.
P2Y12 inhibitors
An interaction of adenosine diphosphate (ADP) with the platelet P2Y12 receptor is a vital part of platelet aggregation. The P2Y12 receptor is the predominant receptor involved in the ADP-stimulated activation of the glycoprotein IIb/IIIa receptor.3,4
Novel anti-aggregating agents, such as prasugrel, ticagrelor and clopidogrel, target the platelet ADP 2 receptor. They induce irreversible platelet aggregation by binding to the ADP receptors present on the platelet surface.5,6
Mechanism of action
Oral P2Y12 inhibitors, such as prasugrel, ticagrelor and clopidogrel are pro-drugs that require an enzymatic transformation in the liver to their respective active metabolite. These medications inhibit platelet aggregation irreversibly.
Cangrelor (Kengreal) is an intravenous, direct-acting, reversible P2Y12 inhibitor. It is an active drug not requiring metabolic conversion and has a rapid onset and offset of action. Cangrelor was approved by the FDA in June 2015 for intravenous application. It is a P2Y12 platelet receptor antagonist that inhibit the release of ADP from damaged blood vessels red blood cells, leading to inhibition of platelet aggregation.
Dental considerations
The risks, and protocol to follow, for patients taking P2Y12 inhibitors are the same as for a patient on ASA. A general agreement exists not to alter treatment regimens in most cases. The risk of modifying the intake of anti-platelet medications outweighs the consequences of prolonged bleeding, which can be managed with local measures.7 Dentists may encounter patients taking P2Y12 inhibitors alone, or in combination with ASA. Various studies have been conducted demonstrating the safety of dental extraction in patients being treated with oral P2Y12 inhibitors where the dose was neither altered nor stopped.8,9
Protocol
According to the Scottish Dental Clinical Effectiveness Programme (SDCEP) guidelines for oral surgery in patients on anticoagulant therapy, the following should be observed:10
The procedure should be planned early in the day and week;
A local anaesthetic solution with a vasoconstrictor should be administered, preferably via infiltration or intra-ligament injection;
The surgical procedure should be performed the least trauma possible, followed by local pressure, which can be adequately maintained by using gauze.
Packing haemostatic agents into the socket, along with suturing of the socket, is advocated.
A 5% solution of tranexamic acid, used as a mouthwash in anticoagulant-treated patients undergoing oral surgery, can be prescribed to be used four times a day for 2 days.
Vitamin K antagonists
Vitamin K antagonists are one of the most frequently used drugs globally. They inhibit the enzyme, vitamin K epoxide reductase, thereby exhibiting their anticoagulant effect. They are indicated in long-term anticoagulation therapy.
Warfarin
Warfarin is a pharmacologically potent compound derived from a plant. It is the most commonly used anticoagulant worldwide.11 The name warfarin is a derivative of WARF (Wisconsin Alumni Research Foundation) and –arin from coumarin.12 It has been estimated that in the UK, at least 1% of the general population, and 8% of the population older than 80 years take warfarin regularly.13
Mechanism of action
Warfarin interferes with the hepatic carboxylation of coagulation factors that are dependent on vitamin K. These include coagulation factors II, VII, IX and X and protein C and S. Warfarin consists of a racemic mixture of two active enantiomers, both of which require necessary biotransformation by the liver. The CYP isoenzyme system has been recognized as an effective catalyst system responsible for this.14 The anti-thrombotic effect is observed when there is sufficient depletion of prothrombin (half-life of 60–72 hours).15
Protocol
Warfarin has been the most debated drug in dental publications, especially concerning dental extractions and minor oral surgeries. The recommendations and protocols have been continuously modified. The protocols have ranged from hospitalization for withdrawal of warfarin and, subsequently, heparinization, to simply monitoring the INR with or without local haemostatic measures post-dental extraction. Simple extraction of teeth in patients on warfarin can be performed safely without a high risk of bleeding provided that INR is ≤3.5 on the day of extraction.10,16
Local haemostatic measures, which include anti-haemorrhagic agents, tissue adhesives and sutures, are recommended. If the INR is ≥3.5, then the treating physician should be informed about the condition and dental extractions should be avoided.10
Direct oral anticoagulants
Recently, in the USA and many European countries, including Italy, three kinds of direct oral anticoagulant (DOAC) have been approved. These include apixaban and rivaroxaban, which act as factor Xa inhibitors (FXaI) and dabigatran, which functions as a direct thrombin inhibitor (DTI). Edoxaban, another FXaI, has also been approved for use in Europe by the European Medicines Agency.17 These drugs have a relatively fast onset and can reach their peak concentrations in just a few hours.18 Additionally, they also have a wide therapeutic margin, fewer drug–drug interactions, and no substantial food interactions.19,20
The advanced diffusion of DOACs has a direct effect on various dental specialties, especially in a surgical context. Owing to their recent discovery and approval, studies on patients taking DOACs undergoing dental treatment are available only from 2012. There are no data yet on the dental management of patients, taking edoxaban.17Figure 1 shows the intrinsic, extrinsic and common coagulation pathways.
Figure 1. Classical pathway model of coagulation. The classical coagulation pathway model. Two pathways, extrinsic and intrinsic, merge in the common pathway at factor X (FX) level. Core coagulation tests activated partial thromboplastin time (aPTT) and prothrombin time (PT) results are interpreted using this model.
Dabigatran
Dabigatran belongs to a class of drugs that directly bind to thrombin, blocking its effects. They are called direct thrombin inhibitors (DTIs). Dabigatran etexilate is the first approved orally administered DTI in the USA.21 A reduction in the risk of stroke and systemic embolism in patients with non-valvular atrial fibrillation was the first FDA-approved indication for dabigatran. Dabigatran had no specific antidote until 2011;22 however, idarucizumab has now been approved as an antidote.23 It is a monoclonal antibody fragment that specifically binds to dabigatran and reverses its anticoagulant activity.24
Mechanism of action
It binds with the active site of the thrombin molecule (IIa), inhibiting the catalysis of fibrin from fibrinogen. Dabigatran inhibits both clot-bound and free thrombin, unlike warfarin.25
Dental considerations/risks
Many studies demonstrate the risk of haemorrhage to be similar to that of warfarin among patients taking DTIs. This is so when the INR value ranges between 2 and 3, excluding gastro-intestinal bleeding.26,27
For patients who need minor oral surgical procedures, such as simple extraction, apicectomy, incisional or excisional biopsies of localized mucosal abnormalities or localized periodontal surgery, the risk of bleeding is presumed to be comparable to someone taking vitamin K antagonists with an INR ≤3.10,28
Protocol
The onset of action of dabigatran is rapid (approximately 2 hours) and it has a short half-life (11.5 hours). It is recommended that all dental procedures be scheduled as late as possible after the most recent dose, ideally after more than 12 hours.
For single uncomplicated tooth extractions, local haemostatic measures, such as mechanical pressure, suturing and topical haemostatic agents (such as Gelfoam or Surgicel) should be adequate to control the bleeding.10
Once the surgery has been completed, local haemostatic measures, for example, suturing, cellulose mesh, gelatin sponge, and tranexamic acid mouth wash (twice daily for 3–5 days) may aid in regulating post-operative bleeding.24 Although there is no direct interaction with NSAIDs, prescription of NSAIDs should be avoided as they cause an increase in the risk of bleeding.28 Alternative analgesics, such as paracetamol, may be prescribed. The antidote for dabigatran is idarucizumab, which rapidly reverses the effects of dabigatran in bleeding patients and in those undergoing urgent procedures.
Apixaban
Apixaban was approved in 2012 by the EMA for use in the prevention of ictus and systemic clots in adult patients with non-valvular atrial fibrillation. It is a reversible and potent factor Xa inhibitor, which is consumed orally. Apixaban has similar therapeutic indications as dabigatran and rivaroxaban.29
Mechanism of action
Apixaban is a strong, effective and reversible factor Xa inhibitor indirectly inhibiting platelet aggregation induced by thrombin. It prevents the formation of thrombin and, hence, clot formation. Whether in its soluble form or bound to the prothrombinase complex, it attaches itself to the active site of factor Xa, consequently, interfering with its interaction with thrombin.30 The drug is absorbed rapidly, and its maximum concentrations are reached at 3–4 hours after administration. Its binding to human plasma proteins is approximately 8%, and it has a half-life of 8–15 hours.31
Protocol
Low-risk procedures, such as simple extractions, mucogingival surgical procedures (if the haemorrhage is not very extensive) and surgical procedures lasting less than 45 minutes can be carried out 12 hours after the last administration of apixaban, or at 24 hours if a dose is missed.10,32
For invasive procedures, apixaban must be suspended for at least 24 hours prior to a procedure with a medium risk of bleeding and at least 48 hours if high risk. Owing to the short withdrawal time, no replacement therapy with low molecular weight heparin is necessary. If the period of drug suspension is prolonged, the administration of low-molecular-weight heparin (LMWH) is recommended.10,33
Heparin, an indirect anti-coagulant, activates anti-thrombin. In the unfractionated heparin (UFH) form, it has a molecular weight of 5000–30,000 Da and is a highly sulphated mucopolysaccharide. Enzymatic or chemical depolymerization is used to derive LMWH from UFH. The mechanism of the anticoagulant action of LMWH is similar to that of UFH, with a longer half-life, more predictable pharmacodynamic and pharmacokinetic properties, and with less risk for haemorrhagic adverse effects.9Figure 2 shows the management strategy for patients with anticoagulation therapy scheduled for invasive dental treatment.
Figure 2. Management strategy for the patient with anticoagulation therapy scheduled for invasive dental treatment. INR: international normalized ratio; OAC: oral anticoagulant; LMWH: low-molecular-weight heparin.
Local haemostatic measures should be carried out after completion of surgical procedures irrespective of the level of risk.
For major oral surgery, or in patients with bleeding comorbidities, the drug should be suspended 24 hours prior to surgery and then restarted once haemostasis has been achieved. This requires around 24 hours.33
Bisphosphonates (BPs) and denosumab
Bisphosphonates (BPs) are bone modifying agents (BMAs) that interfere with bone turnover, mainly through their influence on osteoclasts.34 In the contemporary pharmacological arsenal, they are the primary drugs used against osteoporosis, malignancies metastatic to bone, Paget's disease, multiple myeloma35 and associated skeletal conditions, such as osteogenesis imperfecta and low bone density.36 However, the association of bisphosphonates with osteonecrosis of the jaw, low bone turnover conditions resulting in pathological fracture, and a heightened incidence of atrial fibrillation has increased the scrutiny of their widespread use.37 Recently, denosumab was added to the list of BMAs.38,39 It has similar clinical applications as the BPs, but it is not prescribed for treating multiple myeloma.40
Mechanism of action
Bisphosphonates are either nitrogen-containing (NBPs) or non-nitrogen containing (non-NBPs). Both types indirectly act as anti-resorptive medications. NBPs bind to the calcium in bone. The calcium is ingested by the osteoclast, which is impregnated with NBPs. NBPs impair the mevalonic acid pathway and thus interfere with the bone resorption process. They impair the ability of osteoclasts to form the ruffled border, to adhere to the bony surface, and to produce the protons necessary for continued bone resorption. Non-NBPs replace the terminal pyrophosphate of osteoclasts' ATP and destabilize the energy production of the cell, apoptosis is initiated.35
Denosumab acts as a receptor activator of nuclear factor kappa-B ligand (RANK-L) inhibitor, which occurs as a fully humanized antibody against RANK-L. It acts by inhibiting osteoclast activity and related bone resorption.38
Medication-related osteonecrosis of the jaw (MRONJ)
Bisphosphonates and denosumab, in addition to anti-angiogenic drugs, such as monoclonal antibodies and tyrosine kinase inhibitors, have been identified as drugs that are responsible for medication-related osteonecrosis of the jaw (MRONJ).41
Dental considerations
A comprehensive oral evaluation and comprehensive dental treatment are suggested before commencing BMA therapy to reduce the risk of MRONJ development.42 The incidence of MRONJ in the osteoporosis patient population is very low, estimated at 1–90 per 100,000 patient-years of exposure. However, in the oncology patient population, MRONJ prevalence has been estimated to be as high as 18.6%.43 The majority of patients encounter this bone pathology after dental treatment.43 Therefore, if the systemic circumstances allow, a crucial decision involving the treating physician, dentist and other specialists must be taken to defer the commencement of anti-resorptive therapy until dental health is either improved or treated.44,45 Patients should also be informed about the risk of developing MRONJ, and the significance of maintaining proper dental health.42,46
Dental procedures that involve direct osseous trauma, such as dental extraction or dental implants, must be avoided in asymptomatic patients during active BMA therapy. Removal of the crown and endodontic therapy of the remaining roots may be the most suitable treatment for any non-restorable teeth.47
If systemic conditions allow, discontinuation of oral bisphosphonates for at least 2 months before dental surgery should be considered in those patients who have received an oral bisphosphonate. BMA therapy should be resumed after the osseous healing has taken place.40,42 Treatment goals for patients having established MRONJ include pain elimination, controlling the hard and soft tissue infection and curtailing the advancement and development of bone necrosis.42Figure 3 depicts the algorithm for dental management of patients treated with oral bisphosphonates.
Figure 3. Algorithm for dental management in patients treated with oral bisphosphonates
Disease-modifying anti-rheumatic drugs (DMARDs)
DMARDs belong to a class of drugs used in various arthritic conditions for arresting the advancement of disease, as well as eliminating associated pain. They have an important role in the treatment of rheumatoid arthritis (RA), psoriatic arthritis, Crohn's disease, myasthenia gravis, and juvenile idiopathic arthritis. Cardiovascular side-effects associated with COX-2 inhibitors and short-term action associated with glucocorticoids resulted in the development of newer DMARDs. Presently, non-biological DMARDs such as sulfasalazine, azathioprine, methotrexate, and hydroxychloroquine reduce pain and prevent the progression of the disease. Biological DMARDs, including infliximab, abatacept, adalimumab, golimumab, and tocilizumab, have proved to be more efficient. They exhibit fewer side-effects than non-biological DMARDs; however, they are expensive.48
Mechanism of action
They act against inflammation through different mechanisms, including inhibition of tumour necrosis factor (TNF), suppression of TNF-α and interleukin-1, induction of inflammatory cell apoptosis by increasing chemotactic factors, inhibition of purine synthesis, purine or pyrimidine metabolism.48Figure 4 shows the mechanism of action of DMARDs.
Figure 4. Mechanism of action of disease-modifying anti-rheumatic drugs (DMARDs).
Dental considerations
It is imperative that the dentist has up-to-date knowledge regarding the medications a patient with RA is currently taking, their interaction with other medications, and possible adverse effects. The most common side-effects of DMARDs include gastrointestinal disturbances, alopecia, hepatotoxicity, stomatitis, infrequent myelosuppression, rash and life-threatening pulmonary toxicity. The dentist must evaluate the patient's current medication schedule to avoid any complications prior to prescribing DMARDs, especially in patients with a history of peptic ulcers or renal impairment.49 Although stomatitis is a relatively less severe side-effect of methotrexate, its severity may be reduced by folic acid.50
Dental management of the patient receiving disease-modifying anti-rheumatic drugs (DMARDs)
Before dental treatment:
When indicated, administer antibiotic prophylaxis owing to immunosuppression;51
When indicated, administer glucocorticoid replacement therapy;
Evaluate the potential risk of haemostasis impairment.
During dental treatment:
Identify and treat medication-related gingival overgrowth and ulceration;
Identify and treat xerostomia-related complications;
Identify and treat disease-associated periodontitis.
After dental treatment:
Assess the patient's current medication schedule to avoid any drug interactions and complications;
Instruct the patient to improve oral hygiene.
According to the American Dental Association and the American Association of Orthopedic Surgeons,52 for patients who are currently receiving DMARDs and have had surgically replaced prosthetic joints, prophylactic therapy before invasive dental surgery may be mandated.
The following are the dental procedures for which antibiotic prophylaxis is mandatory:
Implant placement;
Dental extraction;
Re-implantation of an avulsed tooth;
Endodontic therapy beyond the apex;
Initial placement of orthodontic bands (not for brackets);
Intra-ligament local anaesthetics;
Teeth scaling where bleeding is anticipated
Conclusion
The authors have endeavoured to compile a list of drugs (Table 1) to ease their understanding, the oral risks, dental considerations and the management of such patients in a dental set up (Table 1). We hope that the Table will be a handy tool for quick reference, but further specialist consultation/reference must be considered in all cases.
