It is estimated that the average dentist administers between 1500 and 2000 injections of local anesthesia each year. By definition, therefore, every dentist is an expert in the field of local anesthesia, which is an extremely good thing, since without the ability to produce profound numbness, modern dentistry would be all but impossible.
Surprisingly, the first local anesthetic was Cocaine which was isolated from coca leaves by Albert Niemann in Germany in the 1860s. The very first clinical use of Cocaine was in 1884 by (of all people) Sigmund Freud who used it to wean a patient from morphine addiction. It was Freud and his colleague Karl Kollar who first noticed its anesthetic effect. Kollar first introduced it to clinical ophthalmology as a topical ocular anesthetic. Also in 1884, Dr. William Stewart Halsted was the first to describe the injection of cocaine into a sensory nerve trunk to create surgical anesthesia. Halsted was an eminent surgeon who had been trained in Britain. He was the first to establish formal surgical training for physicians in America. Prior to that time, surgery was a self taught discipline among US physicians. He also invented and pioneered the use of rubber gloves. Unfortunately, much to his own regret, he began to use cocaine himself and became highly addicted to it. At that time, there was no stigma attached to the recreational use of cocaine, and it gained a following among the elites of the day. Arthur Conan Doyle's Sherlock Holmes was supposed to be an addict, and Holmes kept Dr Watson around as a source for his drugs, as well as for the comic relief he provided.
It became fairly obvious fairly quickly that while the anesthetic characteristics of cocaine were desirable, the euphoria and subsequent addiction it produced was not! The turn of the century was a tremendous time of scientific progress, and the new discipline of organic chemistry enabled the synthesis of the first analog of cocaine in 1905. (An analog of a chemical molecule is one in which the original molecule is progressively modified to retain and enhance certain holistic characteristics of the original substance while ridding it of other unwanted characteristics.) The first synthetic local anesthetic was procaine, better remembered today by its trade name, "Novocain".
Novocain was not without its problems. It took a very long time to set (ie. to produce the desired anesthetic result), wore off too quickly and was not nearly as potent as cocaine. On top of that, it is classified as an ester. Esters tend to have a very high potential to cause allergic reactions. It is estimated that about one third of all persons who received it developed at least minor allergic reactions to it. Faced with the legal and ethical difficulties associated with the use of cocaine as a local anesthetic, and with the inefficiencies and allergenicity associated with the use of procaine, it is not surprising that most dentists of the day worked without any local anesthetic at all. (Nitrous oxide gas was available during this period.) Today, procaine is not even available for dental procedures.
The first modern local anesthetic agent was lidocaine (trade name Xylocaine®). It was invented in the 1940s. Prior to its introduction, Nitrous oxide gas (plus alcohol in the form of whiskey) was the major source of pain relief during dental procedures. Lidocaine proved to be so successful that during the 1940s and 1950s the use of Nitrous oxide gas as a primary anesthetic agent all but vanished. (Whiskey somehow survived, but it is no longer used on patients.) Today, nitrous oxide is used principally as an anti-anxiety palliative. Lidocaine is in a broad class of chemicals called amides, and unlike ester based anesthetics, amides tend to be hypoallergenic. It sets quickly and when combined with a small amount of epinephrine (adrenalin), it produces profound anesthesia for several hours. Lidocaine is still the most widely used local anesthetic in America today.
Over the next thirty years, a number of other amide local anesthetics were invented, most not differing significantly from lidocaine. The major problem with lidocaine and its analogs is that they cause vasodilation, or the tendency of the local blood vessels to open wider increasing the blood flow in the area. This causes the anesthetic to be absorbed too quickly to take effect. Hence these anesthetics are always mixed with low concentrations of epinephrine which has the opposite effect (ie vasoconstriction) and closes the blood vessels down to keep the anesthesia in position long enough to produce long lasting numbness.
Mepivicaine (Carbocaine®) and prilocaine (Citanest®) have much less vasodilative qualities and hence can be used without the epinephrine vasoconstrictor. The advantage to this is that these anesthetics can be used more safely in patients who are taking medications which may interact negatively with the vasoconstrictor. These drugs include certain blood pressure medications (most notably beta blockers and MAO inhibitors), tricyclic antidepressants (Elevil® and imipramine are two examples) and thyroid replacement hormones (Synthroid®).
How a nerve fiber transmits an impulse
Nerves are NOT like electrical wires with electrons traveling their length to transfer information from one end to the other. They are actually complex electro-chemical structures which utilize the electrical potential difference between the fluid inside of the axon, and the fluid that surrounds the axon. The fluid inside the axon (called cytoplasm) contains a high concentration of potassium ions, while the fluid outside contains a high concentration of sodium ions. There is no real difference in electrical potential between a potassium ion and a sodium ion, however, the fact that they exist in different concentrations on either side of the cell membrane sets up an electrochemical pressure gradient between the two. Sodium ions want to flow into the nerve cytoplasm, while the potassium ions want to flow out, but both are prevented from doing so by the presence of the nerve cell membrane.
When a nerve is stimulated, this sets up a chain reaction in which sodium ions begin to penetrate through the nerve cell membrane and flow into the axon, while potassium ions begin to flow out. This activity happens at the nodes of Ranvier. This process is called depolarization of the nerve membrane. The imbalance in the chemical makeup of the extracellular fluid then causes an imbalance in the concentration of sodium ions at the adjacent node which stimulates an identical depolarization at this node as well. This process proceeds from node to node until the impulse reaches the cell body of the nerve in the ganglion where it stimulates a similar cascade in a network of other neurons which make contact with it.
You might think that once all the potassium and sodium ions have exchanged places, the nerve would no longer be able to conduct impulses. The nerve, however, is a living entity and can regenerate the original concentrations of ions using energy from the food you eat in almost the same way that muscle cells use that same energy to cause muscle movement. It does this using proteins embedded in the cell membrane which act as "ion pumps".
Local anesthetics work to block nerve conduction by reducing the influx of sodium ions into the nerve cytoplasm. If the sodium ions cannot flow into the neuron, then the potassium ions cannot flow out, thus inhibiting the depolarization of the nerve. If this process can be inhibited for just a few nodes of Ranvier along the way, then nerve impulses generated downstream from the blocked nodes cannot propagate to the ganglion. In order to accomplish this feat, the anesthetic molecules must actually enter through the cell membrane of the nerve. Herein lies the differences in the potency, time of onset and duration of the various local anesthetics.
The diagrams above show the essential structures of the two major types of local anesthetic agent; the molecule shown in the left diagram represents the structure of procaine (Novocain). The chain that connects the benzene ring on the left with the amide tail on the right is an "ester linkage". The diagram to the right represents lidocaine and its analogs. The connecting chain in this case is called an "amide linkage". The amide linkage contains an extra nitrogen to the left of the C=O (carboxyl) group.
All local anesthetics are weak bases. They all contain: 1. an aromatic group (the benzene ring seen on the left side of both structures above); 2. an intermediate chain, either an ester or an amide; and 3. an amine group seen on the right side of both molecular structures above. The characteristics of any given anesthetic is determined by the exact structure and relationship of each of these three components. The aromatic ring structure is soluble in lipids (The nerve cell membrane is made of a lipid bilayer and thus the aromatic ring is important in making it possible for the anesthetic molecule to penetrate through the nerve membrane. The amino structure (seen on the right side of the molecules diagramed above) is soluble in water which is what makes it possible for the anesthetic molecule to dissolve in the water in which it is delivered from the dentist's syringe into the patient's tissue. It is also responsible for allowing it to remain in solution on either side of the nerve membrane. The trick that the anesthetic molecule must play is getting from one side of the membrane to the other.
Every cell in the body has a membrane which separates that cell from other cells, and from the extracellular fluids that surround it. The membrane has a definite chemical structure which creates a stable two dimensional sheet which naturally retains its structure in aqueous (water based) solution. It is composed of a bilayer of phospholipid molecules arranged as shown in the diagram above. Each phospholipid molecule is composed of two components; a phosphate radical (shown as a blue ball) which tends to carry an electrical charge, and therefore likes to associate with water molecules, and two long hydrocarbon chains (green) which do not carry a charge and therefore tend to associate with each other in order to avoid contact with the surrounding water molecules. (Not unlike oil, which does not mix with water either). The stability of this structure is based on the fact that the phosphate radicals face outward into the surrounding medium. They are soluble in water and mix well with it. On the other hand, the lipid tails are hydrophobic and avoid contact with the water relying on the phosphate radicals to "protect" them. The lipid tails mingle with each other in the same way that the pioneers used to "circles the wagons" in order to protect themselves. This maintains the structural integrity of the membrane. This super stable micro structure is perhaps one of the most important chemical structures in all of creation because it enables the formation of discreet biological elements separated into cellular components.
While the phospholipid bilayer defines an essentially two dimensional sheet, it actually has a third dimension meaning that it has thickness. In addition, the bilayer is essentially a non aqueous liquid, and as such, other structures such as proteins can be embedded within it, floating around in this miniature ocean of phospholipids. The proteins can have complex shapes and functions depending upon the structure programmed for them by the genetic machinery of the cell. It is thought that the ionic channels that the allow the influx of sodium ions, as well as the efflux of potassium ions during depolarization of the membrane are actually complex protein structures embedded in the neuron membrane.
This section is quite conceptually difficult because it involves some essential chemistry, but it makes for very rewarding reading because it will enable the reader to understand the differences between the common local anesthetic solutions. It will help to explain the reasons that some anesthetics take longer to set than others, and why some cause more prolonged anesthesia than others.
Synthetic anesthetics are prepared as weak bases and during manufacture, precipitate as powdered solids. These solids are poorly soluble in water. They are therefore combined with an acid to form a salt which can be combined with sterile water or saline. The salt dissolves to produce a stable solution which is injectable. The PH (the acid/base balance) of the solution is adjusted to complement the specific molecular structure of the anesthesia in question. Remember that the lower the PH, the more acidic the solution is, and the higher the PH, the more alkaline (basic) it is.
In any given solution of anesthetic, the molecular structure shifts between two forms; an uncharged base molecule (RN) and a positively charged cation (RNH+). ("R" stands for the chemical term "radical" and is the symbol for the generic molecular structure, whether it carries a charge or not.) These two forms of the anesthetic molecule exist in an equilibrium dependent upon the exact PH of the solution:
As the solution becomes more acidic (lower PH), the concentration of hydrogen ions increases. These positively charged ions combine with the uncharged anesthetic radical (molecule) shifting the above equation to the left, and producing a higher proportion of charged cationic structures. As the PH rises, (ie. the solution becomes more alkaline) there are fewer positively charged hydrogen ions. Thus the charged radicals tend to release their hydrogen ions into solution and the equation shifts to the right producing more of the uncharged base.
The PH that produces an equal number of uncharged basic molecules (RN) and charged cationic forms (RNH+) is called the PKa. This is important because the molecular form of the anesthetic that is able to diffuse through the lipid membrane of the nerve cell is the uncharged (RN) form, while once inside the neuron, the active form that inhibits sodium influx is the charged cationic (RNH+) form. As more and more of the uncharged base diffuses through the membrane, the concentration of the uncharged base outside the membrane goes down and the formula re-equilibrates forming more of the uncharged base from the newly higher concentration of positive cations. This continues until all the base eventually diffuses from the outside of the cell membrane to the inside. Once inside the cell membrane, the formula shifts to the left recreating the original concentrations of positive and negatively charged base molecules.
The PH of normal body tissue is 7.4. In situations in which there is an active infection present, the tissue PH can be considerably lower, in the vicinity of 5 or 6. This very reduced PH shifts the equation (outside of the nerve cell) to the left reducing the number of neutral (RN) radicals available to diffuse through the nerve cell membrane. This accounts for the difficulty in anesthetizing such an area. The relative difference between the PKa of the anesthetic and the PH of the body tissue can make quite a large difference in the percentage of anesthetic that is available to diffuse immediately through the nerve membrane, and thus on the amount of time it takes for the anesthetic effect to be felt. The table below shows the PKa and other vital statistics of the seven most commonly used dental anesthetics:
When an anesthetic solution is injected into healthy tissue, it eventually takes on the PH of the surrounding tissue which is 7.4. This is why the third column labeled "% RN at PH 7.4" is important. Remember that only the uncharged basic RN radical can penetrate the lipid membrane components. The higher this percentage is, the quicker the anesthetic penetrates the membrane.
Just because only, say, 18% of an anesthetic solution is available to diffuse through the cell membrane at any one time, this does not mean that all the anesthetic molecules cannot eventually diffuse into the nerve cells. As the number of RN radicals decreases outside of the nerve cell because of absorption, more of the cationic form (RNH+) converts to the RN form to maintain the dynamic balance between the two forms. A low tissue PH simply delays the process. Unfortunately, as the time of onset increases, the chances of the unused anesthetic being absorbed into the blood stream increases, which is why procaine was abandoned as soon as lidocaine became available. It simply "wore off" before it had a chance to enter the nerve and take effect.
Once the molecules diffuse through the membrane, the neutral base (RN) is once again subject to the PH dependent equation above, and many neutral RN radicals shift back to their cationic form (RNH+) to maintain the dynamic balance inside the neuron. Once inside the nerve cell, the active component that combines with the sodium ion channels is the acidic cation form (RNH+).
The irony of this situation is that now the slowest diffusing anesthetic (Bupivicaine with only 18% available to diffuse through the membrane) has the distinct advantage of being the MOST long lasting anesthetic available, with 82% (100% minus 18%) of the absorbed radicals actively binding with the sodium channel proteins to block their activity! (Procaine doesn't count since it takes so long to diffuse through the nerve membrane that most of it has been reabsorbed by the blood vessels before it ever has a chance to penetrate the nerve membrane.) Bupivicaine (Marcaine®) is used today for prolonged surgical operations as a way of maintaining numbness for many hours after the procedure to help reduce postoperative pain.
No matter how quickly an anesthetic agent can enter a nerve, the local blood vessels begin to absorb the unused anesthetic as soon as it is injected. In order to slow this process down, manufacturers of these solutions add a substance that in low concentrations acts to cause the local blood vessels to constrict, or narrow down. This restricts the amount of blood and plasma entering and leaving the site of the injection which has the net effect of slowing the vascular absorption of the anesthetic solution. This keeps the unused anesthetic solution in place longer and prolongs the action of the drug. The substance used to do this is called a vasoconstrictor (vaso refers to blood vessels and constriction means to close down). The vasoconstrictor used is the naturally occurring hormone epinephrine or one of its analogs called levonordefrine. Epinephrine is an ideal vasoconstrictor because it is manufactured naturally by the body as adrenaline, sometimes called the "fight or flight hormone". In addition to causing a constriction of blood supply, if it enters the general circulation it can cause an increased heart rate and stronger heart beat, along with a feeling of nervousness. These side effects account for the "rush" that some people feel after receiving an anesthetic shot.
All anesthetic solutions are sold with added vasoconstrictor. Only two, mepivicaine and prilocaine are sold with or without vasoconstrictor. Mepivicaine and prilocaine have the advantage of producing only minor vasodilation and, though both are short acting without their vasoconstrictor added, they still produce adequate anesthesia for short procedures. The major advantage of using an anesthetic without a vasoconstrictor is that there are virtually no interactions with other drugs the patient may be taking. Vasoconstrictors may not be used with certain types of blood pressure medications, artificial thyroid hormones, or tricyclic antidepressants.
Vasoconstrictors are also not used in any body area in which the blood supply must "double back" on itself. This includes such blind ended appendages as the tip of the nose, or the fingers or toes. In these areas, a vasoconstrictor may block all blood flow to the appendage causing tissue necrosis (death of the tissue).
The use of vasoconstrictor does carry one additional penalty for the practitioner. These naturally occurring hormones are not very stable, and must be stabilized by the addition of an acidic preservative. The presence of the preservative can lower the PH of the anesthetic solution to the range of 3.8 to 5.0, thus reducing the amount of the neutral basic radical (RN) and slowing the onset of action of the anesthetic. This effect is, thankfully not especially significant, and anesthesia with vasoconstrictor is far and away the most popular choice among practitioners when other clinical considerations permit its use.
The maximum dose for local anesthetic solutions is somewhere between 70 mg to 500 mg. Of course, the miximum dose is dependent upon the age and health of the patient, the type of solution used, and whether vasoconstrictor is present or not. These anesthetic agents are distributed in concentrations that are appropriate to their toxicity and their anesthesia producing qualities. All dental anesthetics that are distributed with vasoconstrictor (with the exception of bupivicaine, prilocaine and articaine which will be covered later) come in 2% concentrations. Mepivicaine without vasoconstrictor is distributed in 3% concentration. The carpules (cartridges) that these drugs are distributed in contain 1.8 ml of solution (Articaine carpules contain 1.7 ml).
Since people vary in age, weight and health, the maximum dose of any given drug that any individual can tolerate varies widely and can be computed arithmetically. The maximum dose (for a normal adult 150 pounds and up) for Articaine and lidocaine is 500 mgm. The maximum dose of mepivicaine and etidocaine is 400 mgm. The maximum dose of prilocaine is 600 mgm, and the maximum dose of bupivicaine is 90 mgm. A 2% solution contains 20 mg of anesthetic agent per milliliter which means that each 1.8 ml cartridge contains 36 mg of agent. In the case of lidocaine, this works out to about 13 carpules delivered at one time. For children, it works out to about 1/3 to 1/2 that number depending on their weight. These doses are not considered lethal. They are simply the doses at which some people begin to feel toxic systemic effects from the drugs which may include CNS (Central Nervous System) effects of sedation, light headedness, slurred speech, shivering or twitching or, in rare cases, seizures; or cardiovascular effects such as hypotension (low blood pressure). The incidence of toxicity to local anesthetics in the dental setting is extremely rare and generally revolve around very unusual patient centered physiologic abnormalities rather than poor anesthetic technique on the part of the dentist. The most frequent dose related toxic effect in the dental setting is nervousness and high heart rate, due not to the effect of the anesthetic itself, but rather to the systemic effect of the vasoconstrictor.
Three special cases
Bupivicaine is a special case in dental anesthesia. It is used mostly by surgeons who want to produce very long acting anesthetic effects in order to delay the post operative pain from their surgery for as long as possible. Bupivicaine comes in 0.5% solution with a vasoconstrictor. It is the most toxic of all the anesthetic agents and this toxicity is reflected in its low concentration in the carpules. As noted in the PKa table above, it is has a very alkaline (basic) PKa which means that a relatively low percentage of the uncharged base radical (RN) is available for immediate diffusion through the cell membrane. Thus it takes a fairly long time to set. However, once inside the cell membrane, over 80% of the radicals that do diffuse become available for binding to the sodium channel proteins. This high protein binding ability causes the drug to remain active for a long time once it has diffused through the cell membrane.
Prilocaine has the same general PKa as lidocaine, which means that for all practical purposes it can be used in the same way and at the same concentrations as lidocaine, producing about the same anesthetic affect in the same setting time for the same duration. It is, however somewhat less toxic in higher doses than lidocaine, and thus is delivered in a 4% solution which places about twice as much molecular anesthetic in proximity to the nerve as is the case with lidocaine or mepivicaine. In addition, since it has little vasodilatory activity, it may be used without a vasoconstrictor. The higher concentration of anesthetic agent, in combination with a vasoconstrictor, therefore, gives this anesthetic the twin advantages of fast onset of activity with prolonged anesthetic activity due to the larger number of molecules available to cross the cell membrane. Unfortunately, the toxicity of a single carpule of 4% prilocaine is still greater than the toxicity of a single carpule of 2% lidocaine which means that fewer carpules can be used before toxic levels are reached.
Articaine is the newest addition to the local anesthetic arsenal and was approved by the Food and Drug Administration in April 2000. It has been in use in Europe since 1976 and in Canada since 1983. Its approval in the US has been delayed by the FDA due to the presence of a preservative which the agency said was unnecessary in single use carpules and was a potential allergen. It was approved when the French company Septodent finally removed the preservative from American shipments.
Articaine has the same PKa and toxicity as Lidocaine, however it is metabolized differently. It has a half life in the body less than 1/4 as long as that of lidocaine and only 1/5 as long as mepivicaine. This means that more of the drug can be injected later in the dental procedure will less likelihood of blood concentrations building to toxic levels. Articaine is formulated in a 4.0% solution with vasoconstrictor. The presence of the vasoconstrictor retards the systemic absorption of the anesthetic allowing higher concentrations of the drug to remain in the area of injection and slowing the absorption into the bloodstream. The higher local concentration of the drug produces a high level of the uncharged radical (RN) to be present at the membrane which brings about very rapid absorption of the drug. In addition, the benzene ring on the left end of the molecule has been replaced with a thiophene ring. This modification allows for faster and more complete absorption through the nerve cell membrane. The ability of this drug to penetrate barriers is so great that it has been used to penetrate thick bone to produce anesthesia in a way that other anesthetics cannot. Articaine has become the local anesthetic of choice in most countries into which it has been introduced.
*The presence of vasoconstrictor in the carpules further reduces the advisable maximum dose, if only to avoid systemic annoyances such as the "rush" some people feel when they get too much vasoconstrictor.
For patients who are allergic to local anesthetic
There are two broad classes of injectable local anesthetic. They are the amines and the esters.
Esters were the first class of local anesthetic agent and contain such drugs as Cocaine, Procaine, Tetracaine, Chloroprocaine and Benzocaine. Today, only Benzocaine is routinely used in dental applications, and its use is limited to topical application (applied with a cotton swab prior to injections or for minor procedures). The others are used today mostly in obstetrics and for producing spinal anesthesia. The most well known dental anesthetic was Novocain. Novocain was the brand name for the first procaine injectable produced for dental use. It was invented at the end of the 19th century. It is no longer used in dentistry partly because it has a short duration, and partly because it tends to be highly allergenic. High allergenicity is a trait common to all the ester based anesthetics. In general, a patient known to be allergic to one ester anesthetic tends to be allergic to all ester anesthetics.
Amines were invented later. They include Lidocaine, mepivicaine, Bupivicaine and all the other commonly used anesthetics discussed above. They all have the advantage of very low allergenicity. Almost no one is allergic to these drugs....The operative word is almost!
If you happen to be one of the very few persons who knows he or she is allergic to modern dental anesthetics, you already know how seriously difficult dental procedures can be. But there is actually a lot of hope. Not all allergic reactions are especially serious. A vast majority of patients who are allergic to local anesthetics suffer only temporary generalized itching and skin rash when getting local anesthetic injections. Thus, if you are willing to put up with these symptoms, and your dentist feels comfortable using emergency drugs in case of the rare emergency, the chances are very good that you can have normal dental procedures performed with regular local anesthesia. The American Academy of dermatology has this to say about local anesthetic allergy (emphasis added):
The decision to administer or receive a drug that the patient is known to be allergic to is not a trivial matter. Even though anaphalaxis is quite rare with amine based local anesthetics, it is still possible, and both the dentist and patient must acknowledge and be prepared to deal with the consequences. On the other hand, serious dental pain and poor dental esthetics have real life consequences which may be just as bad for the patient as the possibility of having to deal with the effects of the allergy, no matter the consequences.
The signs and symptoms of allergic reaction include:
However, allergic reactions can have any degree of severity ranging from minor itching to full blown anaphylaxis. In a very serious anaphylactic reaction, the patient may experience serious difficulty breathing due to closing down of the bronchioles in the lungs or swelling in the throat area due to urticaria as well as seriously low blood pressure leading to anaphylactic shock. This set of events, left untreated can lead to death.
Anaphylaxis is, of course the worst case scenario. Fortunately, the majority of allergic reactions to local anesthetics are fairly mild and are easily treated with light antihistamines like diphenhydramine (Benedryl). In a vast majority of situations, patients who have patch tested allergic to all modern local anesthetics can be safely injected for necessary dental work provided the dentist is ready with the appropriate drugs and training necessary to combat an anaphylactic reaction in the unlikely event one should occur. The drugs to have on hand are as follows:
NO!!! Local anesthetic injections before a drug test do not cause false positives! Having said this, there are lots of problems with drug testing, especially as it relates to employee screening in today's large corporate structures. False positives may be the result of a range of problems from cross reaction with over the counter and prescription medications to systemic conditions such as diabetes, or kidney and liver disease. Plain sloppiness on the part of the testing facility may also be a factor.
The following is a list of illegal drugs, each followed by a number of commonly used and legally available substances (many of them prescription drugs) that may cross react and cause a false positive drug test. A positive screening often results in special handling of the specimen using a second, more expensive drug testing regimen, and may be able to screen out even these sources of error, so the fact that a subject is taking legally prescribed drugs or any of the over-the-counter medications listed below may not be sufficient to exonerate the subject if he/she is, in fact using illegal drugs. On the other hand, subjects who believe that their specimen was contaminated by one of the substances below have a right to request that it be retested using a more accurate and substance specific test.
Note that the use of prescription (DEA schedule II, III, IV or V) drugs without a doctor's prescription is illegal and are grounds for the legal consequences stemming from a positive drug test. (Note: schedule I drugs are not legal to prescribe to the general public.)
For more information about false positive drug tests, please click here to go to the AlwaysStayClean website.
If you believe that your specimen has been tested positive in error due to the use of legally prescribed drugs or ones purchased legally over the counter, then you should request retesting of your specimen.
Copyright 2000 Martin S. Spiller, D.M.D.
DISCLAIMER: Statements made on this web site are for informational purposes only and are not intended to be substituted for the advice of a medical professional. Information and statements have not been evaluated by the American Dental Association or any federal regulation agency and are not intended to diagnose, or treat any disease or medical condition. This is a personal website written by an individual dental professional who's intention is to enlighten the public with generally accepted, mainstream medical/dental information. I do not claim to represent the opinions of all dental or medical professionals. No website is a substitute for a visit to a living, breathing dentist or physician who can deal with you personally.