blind researches

BMJ 2003;327:158-160 (19 July), doi:10.1136/bmj.327.7407.158
Education and debate
Separation of anxiety and depressive disorders: blind alley in psychopharmacology and classification of disease

Edward Shorter, professor of the history of medicine1, Peter Tyrer, head of department2

1 History of Medicine Program, Faculty of Medicine, University of Toronto, Toronto ON, Canada M5G 1VJ, 2 Department of Psychological Medicine, Imperial College Faculty of Medicine, St Mary's Campus, London W2 1PD

Correspondence to: P Tyrer p.tyrer@imperial.ac.uk

No new drugs for mood and anxiety disorders have reached the market for over a decade. Why is there so little innovation in a sector that accounts for the largest proportion by far of sales of psychiatric drugs?

The first 150 words of the full text of this article appear below.

The current division between anxiety and depression is increasingly recognised as inadequate. In the community, most mood disorders present as a combination of depression and anxiety. Yet the Food and Drug Administration in the United States, which has become the world bellwether of drug approval, indicates drugs either for major depression or for the various forms of anxiety recognised by the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders (DSM). As a result, the pharmaceutical industry is compelled to develop drugs for diagnoses that are of questionable clinical relevance. This is one reason for the big slowdown in drug discovery in psychiatric drugs. A return to the former unitary classification of mood and anxiety disorders as nervousness or cothymia might represent a way out of this blind alley.

In 1980, the American Psychiatric Association revised its standard system of diagnoses in the third edition of its diagnostic manual . . . [Full text of this article]

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* Langen, B., Egerland, U., Bernoster, K., Dost, R., Unverferth, K., Rundfeldt, C. (2005). Characterization in Rats of the Anxiolytic Potential of ELB139 [1-(4-Chlorophenyl)-4-piperidin-1-yl-1,5-dihydro-imidazol-2-on], a New Agonist at the Benzodiazepine Binding Site of the GABAA Receptor. J. Pharmacol. Exp. Ther. 314: 717-724 [Abstract] [Full text]
* WEICH, S., ARAYA, R. (2004). International and regional variation in the prevalence of common mental disorders: do we need more surveys?. Br. J. Psychiatry 184: 289-290 [Full text]
* Walker, B. F (2003). Risk of suicide remains high fifteen years after deliberate self-harm. Evid. Based Ment. Health 6: 106-106 [Full text]
* Joffe, M. (2003). Separation of anxiety and depressive disorders: Maybe pharmaceutical failure has created culture of niche diagnosis. BMJ 327: 870-870 [Full text]
* Weeks, R. L (2003). Separation of anxiety and depressive disorders: Normal rules of critical evaluation were presumably suspended. BMJ 327: 869-869 [Full text]
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Blind alley or poor reasoning
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Declaration of Interests
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We are responsible too.
Tanuj Sidhartha
bmj.com, 7 Aug 2005 [Full b

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oral cancer

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The facts about oral cancer (signs, symptoms and factors)
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Physical Risk factors (smoking, drinking, age and HPV)
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Epidemiology and mortality
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Leukoplakia and erythroplakia
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Cancer of the lip
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Tumors of the salivary glands
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Malignant melanoma
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Screening for oral cancer
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Visual exam
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Oral CDX
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Vizilit

Oral Cancer--The facts (and why that lump you noticed in the mirror this morning is probably NOT cancer!)
Oral and pharyngeal (throat) cancer represents about 3% to 5% of all forms of cancer. In 2006, 30,000 cases are expected to be diagnosed in the US, and 8000 are expected to die of the disease. If cancer of the larynx, which is quite similar to oral squamous cell cancer and has similar risk factors is includedl, an additional 14,000 diagnoses will be added to the 2006 total.

The five year survival rate for this type of cancer has remained at about 50% since the early 1960's. About half of the cases occur in persons over the age of 65.

Oral cancer attacks more men than women (male/female ratio = 2/1), and more blacks than whites (black/white ratio = 2/1). The survival rate is better for Caucasians (54%) than for Afro-Americans (34%). The most common sites of oral cancer are the floor of the mouth, the sides and undersurface of the tongue, the back of the throat, and the lips. Although it is not considered oral cancer in the strict sense, cancer of the larynx (the voice box) has a similar etiology (cause & origin) and causes approximately 2% of all forms of cancer. 90% of the victims of cancer of the larynx are males, and most are between 60 and 70 years old.

Indications that you may have developed oral or laryngial cancer

* A sore in the mouth that does not heal spontaneously within three weeks;
* A lump or thickening in the cheek;
* A white or red patch on the gums, tongue, or lining of the mouth;
* Soreness or a feeling that something is caught in the throat;
* Difficulty chewing or swallowing;
* Difficulty moving the jaw or tongue;
* Numbness of the tongue or other area of the mouth; or
* Swelling of the jaw that causes dentures to fit poorly or become uncomfortable.

The general characteristics of oral cancer

90% of all oral cancers are of a type called Squamous cell carcinoma, which means that they derive from squamous cells which are the type of cells that make up the pink mucosa that lines the mouth. Laryngeal cancer (cancer of the vocal cords) is also generally caused by squamous cell carcinoma, and is also associated with heavy smoking. Most oral cancers tend to happen on the floor of the mouth or the sides and undersurface of the tongue. They also tend to be relatively painless during their early development. The image to the right shows a rather advanced cancer on the side of the tongue. (Click the image to see a larger version, as well as some other rather scary examples of oral cancer.) Note the mottled white and red appearance of the growth. As you will see, this is an important characteristic of these cancers.

It is interesting to note that squamous cell carcinoma is NOT USUALLY one of the more virulent cancers, and yet it kills about half of those that get it. This is an important point since if it is diagnosed at a reasonably early stage (within the first year, or in some cases within the first two years--The earlier, of course, the better), it can generally be removed before it becomes locally invasive or spreads to other parts of the body and becomes a death dealing issue. Why would anyone let a problem like this progress until it is this large? (Click the image for more info on why this one got so big.) Why does does such a slow growing cancer have such a large mortality rate? (Mortality rate is the measure of the ratio of those who contract the disease to those who die from it. In the case of Squamous cell carcinoma, the mortality rate is about 50%, meaning that approximately half the people diagnosed with it will eventually die as a direct result of the cancer, or from complications associated with it.)

The physical factors that increase the risk of oral cancer

Since 90% of all oral cancers are of a type called Squamous Cell Carcinoma, when we speak of "risk factors" associated with oral cancer, we are talking about risk factors associated with this particular entity. These risk factors do not pertain to the other 10% of cancers which can occur in the oral cavity. This 10% are covered later on this page. There are four factors that appear to increase the risk of developing oral squamous cell carcinoma:

(1)Tobacco AND (2)alcohol--When indulged in together over a long period of time, heavy alcohol and tobacco use are the most potent physical factors contributing to the development of squamous cell carcinoma. Those who both smoke and drink heavily, have a 15 times greater risk of developing oral cancer than those that have neither habit.

* Tobacco is a known carcinogen, which means that it is known to damage cellular DNA. Damaged DNA can cause the cellular reproductive machinery to malfunction, which is the first step in the growth of malignant cellular masses (cancer).
* Alcohol is known to inhibit a gene that functions in response to DNA damage. This gene is responsible for initiating cell death in cells in which the the DNA is damaged.
* Thus the tobacco causes malignant mutations in the cellular DNA, while the alcohol inhibits the body's natural defense against malignancy.

(3)Age--The large majority of squamous cell carcinoma victims are over the age of 45. This probably relates to the tendency of the immune system to become less and less competent at recognizing and eliminating mutated cells that arise in the body from time to time. It may also be associated with the time it takes for the other three factors discussed in this section to have their damaging effects.

(4)HPV--The human papilloma virus. HPV is transferred from person to person by vigorous physical contact, especially oral sexual contact. The presence of HPV may be the major risk factor in the development of oral cancers in patients who are not heavy smokers and drinkers. HPV is covered in more detail under the lifestyle discussion below.

Factors relating to epidemiology and mortality in patients with oral and laryngeal cancers (Epidemiology is the study of how a disease spreads and who is likely to get it.)

Lifestyle issues:

Lifestyle issues are behavior patterns which are considered under the control of the individual. They are the most important factors in the mortality (death rate) and epidemiology (how the disease spreads, and who is likely to get sick) associated with oral and laryngeal squamous cell cancers. Patient lifestyle choices probably accounted for the development of the lesions seen in the images on this page, and also contributed to the fact that they grew so large before diagnosis.

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Heavy Drinking-- While alcohol is one of the major physical risk factors in the direct development of oral cancer, heavy drinking (the behavior) is associated with oral cancer's high mortality (death) rate. Heavy drinkers are much less likely to notice, let alone seek professional help for a painless growth under their tongues!
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Smoking-- Tobacco has a direct effect on the tissues that the smoke actually comes into contact with. This includes both the tissues of the mouth, and the tissues in the larynx (voice box). 75% of persons who develop oral squamous cell carcinoma are, or have been heavy smokers. It appears that the effects of tobacco are cumulative, so people who have been heavy smokers (or snuff dippers) for many years are more at risk for developing oral or laryngeal cancer than those who have only recently started.
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HPV-- When discussing HPV as it relates to oral cancer, the lifestyle issue here relates to sexual behavior. 25% of oral cancers appear in patients who have never smoked, and it is thought that human papilloma virus may be the carcinogenetic element involved in these cases. There are approximately 80 strains of the human papilloma virus. Many of the strains of HPV cause ordinary warts, the kind that develop on the hands and feet. Most strains of HPV are thought to be harmless, but two types, HPV16 and 18, have been shown to be the causative agents of cervical cancer (cancer affecting the epithelial cellular layer--the surface cells--surrounding the opening of the uterus) and are spread by sexual means. These strains of HPV have recently been implicated as a causative agents in oral squamous cell cancer as well. Since the virus itself is transmitted exclusively by vigorous physical contact, the implication is that oral/genital sexual contact (oral sex) may be the major means of transmission of the virus.
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Normal kissing does not seem to be implicated. Monogamous couples composed of persons who have never engaged in sex outside of their relationship are not at risk either.
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As the incidence of smoking has declined over the last 30 years in the USA, the incidence of promiscuous sexual contact has risen. Thus the expected benefit of fewer people smoking has been offset by the liability of more widespread infection with HPV. This means that the rate of oral cancer diagnosis in the US has remained constant over the last twenty years, instead of falling as might have been the expected with the decline in the number of smokers.

For more on the human papilloma virus, please see the website of the oral cancer foundation.

The implication here is that if you are under the age of 45, have not indulged for long periods of time in the combined habits of heavy drinking and smoking, and have not indulged in vigorous oral sexual activity with partners that are likely to be promiscuous, then the likelihood that the sore you found in your mouth this morning is probably not squamous cell cancer. Hopefully, this page should go a long way in setting your mind at ease. On the other hand, this is NO guarantee that the lesion is not dangerous. No website is a replacement for a visit to a dentist or physician who can deal with you personally!

The rule of thumb in assessing any soft tissue sore in the oral cavity is "if it is not gone in three weeks, see a dentist or physician and have it properly diagnosed"!

Age and its relationship to mortality and epidemiology in oral and laryngeal cancers

One of the most important factors associated with oral cancer is age. Even in a population of cigarette smoking drinkers, the vast majority who develop oral cancer tend to be over the age of 40. Half of all oral cancers arise in persons over the age of 65. Advanced age is probably the most important factor in the mortality associated with the development of any cancer. This is due to the fact that as a person ages, their immune system tends to become less efficient at recognizing and eliminating aberrant cellular growths which arise from time to time in people of all ages. Since about half of all cases of oral cancer, and most cases of laryngial cancer occur in patients over the age of 65, the advanced age of the cohort alone would account for a substantial portion of the death rate in these patients.



Painless Lesions contribute to the mortality rate ("Lesions" are abnormal growths, erosions or sores.)

The initial lesions of squamous cell carcinoma tend to be painless. The fact that they are painless makes them easily overlooked in the early stages. The lack of pain in early lesions combined with the tendency for this cancer to develop in heavy drinkers may be largely responsible for oral cancer's 50% mortality rate . These lesions start out as small white or red patches about 1 to 2 mm in diameter and progress toward larger lesions slowly. They will usually be noted by a patient when they are large enough to be felt during movements of the effected organ. They generally appear to be irregular sores with a white and red mottled center, surrounded by a red border. As the lesion enlarges, it may become more and more bound-down to the underlying tissues thus becoming less mobile. Pain and/or numbness generally develop later in the course of the lesion's growth.

Leukoplakia

Persons who smoke heavily or use smokeless tobacco such as snuff and chewing tobacco tend to get whitish patches called leukoplakia on the oral mucosa (the wet tissue lining the mouth) . The image on the right shows a fairly typical patch on the side of a man's tongue. The image to the left shows a similar patch on the floor of the mouth. These patches can happen anywhere in the oral cavity such as on the cheek mucosa, the roof of the mouth, or the back of the throat. The common denominator seems to be HEAVY use of cigarettes or prolonged contact of snuff or chewing tobacco with cheek tissue. Leukoplakia is not itself a form of cancer, but is considered pre-cancerous and should be biopsied (a procedure in which a tiny piece of tissue is sent out for microscopic examination) since about 20% are found to be pre-malignant . It is white, firm tissue and cannot be scraped off. It generally goes away when the stimulation of the tobacco stops, but with continued heavy tobacco use it can transform into squamous cell cancer. In order to picture what a cancer developing in these lesions would look like, imagine irregular red blotches developing inside the white leukoplakic plaque, and a large red border developing around the entire lesion! Erythroplakia (see image at right) is the term applied to red bloches which appear within areas of leukoplakia. Erythroplakia is considered to be more dangerous than leukoplakia alone. Click on the image to the left or the one to the imediate right to see these images enlarged, and other scary images of leukoplakia. Neither leukoplakia nor erythroplakia are contagious conditions.

The number one cancer of the head and neck is cancer of the larynx--the voice box--which is more susceptible to particulate carcinogens such as cigarette smoke and various forms of pollution than other tissues. The majority of patients who get cancer of the larynx are men between 60 and 70 years old who have a history of heavy smoking and generally heavy drinking. Women in the same category are also prone to squamous cell carcinoma.

Cancer of the lip

Cancers on the lips are a special case. They generally strike the lower lip and are more likely to happen after long, repeated episodes of exposure to the sun. Cancer of the lip is also squamous cell carcinoma and has the same clinical course as intraoral cancers. Going to the beach several times a summer is generally not a significant risk factor for cancer on the lip. Most people who get this form of cancer tend to be outdoor workers who labor all day in the sun for years on end. Perhaps because more people work indoors today than ever before, the incidence of cancer of the lip is decreasing.

What about the other 10% that are not squamous cell carcinoma?

The probability of developing any type of cancer increases with age! Chronic illness is another factor that increases the likelihood of developing these forms of cancer. There are, unfortunately, numerous types of cancer that can originate in various oral structures including bone, lymph nodes, salivary glands etc. These are not associated with known risk factors the way squamous cell cancer is associated with smoking, drinking and promiscuous oral sexual activity. There is some evidence that non squamous cell cancers of the oral cavity are related to precipitating factors such as exposure to the Epstein Barr virus (the virus responsible for mononucleosis which in some persons seems able to remain dormant in the body for a lifetime) as well as the human papillomavirus (HPV), and radiation treatments to the head and neck for cancer or acne (not diagnostic x-rays). Radiation was once a treatment modality for facial acne (back in the early 20th century) but is no longer used because of the obvious danger from large amounts of radiation. It is still used in the treatment of carcinomas and Sarcomas (two different classifications of malignancy) but is carefully aimed and metered to avoid side effects.

A minor salivary gland tumor tends to be a firm mass on one side of the palate (the roof of the mouth). They do not occur in the midline. If it is cancerous, it will remain enlarged and will not go away after two or three weeks. About 50% of these large persistent masses will prove to be malignant (cancer). But be aware that small salivary glands in the palatal mucosa do become infected occasionally. When this happens, they can become sore and slightly enlarged, but the problem is generally temporary and disappears without treatment within two weeks.

About 80% of all salivary gland tumors begin in the parotid glands. (A tumor is simply a mass. It is not necessarily cancerous.) The patient notes a swelling on the side of the face below and in front of the ear. This swelling does not get larger and smaller at different times of the day (as salivary gland infections do), but remains constant, or grows larger over time. 10%-15% of salivary gland tumors start in the submandibular glands causing a swelling on one side of the neck just under the jawline. These also remain enlarged over time. The rest develop in the sublingual gland, causing a similar swelling under the chin, or in one of the many minor salivary glands. Most tumors of the parotids are benign (noncancerous). Masses in the minor salivary glands (the smallest of salivary glands) are more frequently malignant (cancerous), however because there are so many more parotid gland tumors, a greater number of cancers are found in the parotid glands than any of the other salivary glands. (For a diagram of the major salivary glands, see my page on Dry Mouth.)

One of the most deadly forms of oral cancer is Malignant melanoma. Thankfully, it is very rare in the oral cavity. It begins as small black spot, generally smaller than a millimeter, and develops irregular borders as it grows larger (see image on the right). Melanoma can happen on any tissue in the mouth, particularly inside the lips, cheeks, undersurface of the tongue and on the hard palate. It is likely to be tan, dark brown or black, sometimes mixed with red or gray.

Melanoma occurring anywhere other than the mouth is generally considered to be fairly treatable. Unfortunately, due to the anatomy of the head and neck, oral melanoma is most often fatal.

Fortunately, most dark spots on oral tissue are likely to be amalgam tattoos discussed in more depth on the sores, lumps and bumps page. Amalgam tattoos happen after dental appointments, remain stable, do not grow larger over time, and are relatively circumscribed (without diffuse, irregular borders). They also tend to have a blue-gray color, unlike the dark brown or black seen in melanoma. They are most common on the gums, cheeks and floor of mouth immediately adjacent to teeth. Amalgam tattoos attain and maintain their maximum size shortly after the introduction of the amalgam into the tissue, while melanomas will grow and change shape over the course of a week or two.

How dentists screen for oral cancer

Although screening by your dentist is the best method of reducing the pain, suffering and mortality related to oral cancers, it is not altogether reassuring to know that differentiating early malignant and premalignant lesions from benign growths is quite difficult, even for experienced dental practitioners. Early stage oral cancers are asymptomatic and the clinical characteristics associated with malignancy such as pain, swelling, redness, enlargement, fixation (becoming bound down to underlying tissue) and deformation of the surrounding tissues generally do not develop until quite late in the clinical course of the disease.

Until recently, there were only two courses a dentist could take when he saw a suspicious early lesion. ("Lesions" are abnormal growths, erosions or sores.) The first, and most frequent course was waiting several weeks to see if the lesion progressed or regressed. If It went away, all was well, and the crisis was averted. If it got bigger, or if the lesion had been present for several weeks and was already of significant size on initial examination, then the dentist proceeded to the second course which is a sectional (knife) biopsy in which the patient is anesthetized and a piece of the lesion is surgically removed and sent to a laboratory in formalin for microscopic analysis. The microscopic examination of the tissue sample provides a definitive diagnosis upon which to base a treatment plan.

The difficulty with this protocol is that there is a high incidence of oral abnormalities which can be candidates for biopsy. It is claimed that between 5 and 15% of all new patients present with abnormal lesions in their mouths, however these include such lesions as aphthous, fibromas and many of the other obviously benign conditions explained on this page. No knowledgeable dentist would consider these to be candidates for biopsy. Even so, quite a few truly suspicious lesions do walk through our doors with only about 5% turning out to be cancer. Given these odds, it is impractical to immediately subject all these lesions to a potentially painful procedure like a surgical biopsy. Thus, using the older protocol, virtually everyone presenting with an early lesion was sent home to wait the obligatory two to three weeks to see if it progressed or not. While not a dangerous course of action, it still left any potential malignancy to progress for the entire waiting period plus whatever time it took to examine the biopsy tissue. It was not especially reassuring for either the dentist or the patient to know that if there was a cancerous lesion, it had to wait at least a month to be removed!
A better screening method has recently become available. It is called the Brush Biopsy (Oral CDx). This consists of placing a small, sterile, hard bristled brush over the lesion and twirling it around until part of surface of the lesion is abraded away. The procedure rakes up cellular material from the entire thickness of the surface of the lesion onto the brush. Although this procedure may irritate the area, (it should produce pinpoint bleeding areas) it does not generally require local anesthesia. The cellular material scraped up on the brush is smeared onto a glass slide, fixed with a chemical that comes with the kit, and dried. The glass slide is then placed into a plastic container and sent to a lab for computer scanning and further manual examination of suspicious cells. The makers of this biopsy kit claim 100% accuracy in identification of abnormal cellular components provided that the clinician was aggressive enough in obtaining a full thickness sample. The brush biopsy does NOT establish a definitive diagnosis. It does indicate the need for a surgical biopsy to establish the diagnosis.

The brush biopsy is not suitable for melanoma ( pigmented lesions) or lesions on the dry parts of the lips. It is generally reserved for use on lesions that show eroded or overgrown mucosal surfaces. Its principle use is for pre-cancerous lesions that will develop into squamous cell carcinoma. It is not useful for deeper lesions such salivary gland tumors.

Vizilite

Zila Pharmaceuticals has heavily marketed a light source which, when shined on oral mucosa is reputed to cause squamous cell carcinoma lesions to fluoresce, thus helping a trained clinician to spot them for early detection of oral cancer. This product is called Vizilite, and it is heavily marketed to dentists. It would be a great benefit for the early detection of oral cancer if......it actually worked as advertised.

In 2004, "the manufacturers of Vizilite applied to the ADA for the ADA Seal of Acceptance for their product. The official seal of acceptance is considered the ultimate in product recognition in terms of marketing a given product for use in dentistry in the United States. The Council on Scientific Affairs is charged with the review of all studies related to products requesting the seal. The companies are asked to submit all studies that support their claims. They are required to submit at least two credible clinical studies.

The usual requirement is that of two independent double blind clinical trials, each conducted at a separate site. In addition to the review of this data by the entire Council on Scientific Affairs, the studies are sent out to a number of outside reviewers. The conclusion on Vizilite was quite clear. Their submitted study data was extremely weak. All outside consultants were in agreement in not supporting the product for the seal. The Council was unanimous in not supporting the application." (Click here for the reference)

This light source has apparently been shown to be beneficial in the differentiation of cervical (uterine) squamous cell carcinoma. It appears, however, that the progression of the same cancer in the oral cavity is biologically different from the progression of cervical squamous cell carcinoma, and for this reason, it is of limited use in the oral cavity.

Therefore, the use of the Vizilite as a method of screening for oral cancer is probably more of an unnecessary expense than a benefit to either patients or the doctors using it.

Even so, the manufacturers of Vizilite continue to heavily market the product, and even advertise in the Journal of the American Dental Association. The presence of an ad in the Journal does not mean that the ADA endorses the product, any more than an ad on this website means that I endorse the product.

oral anatomy

Normal oral anatomy (click the appropriate structure above)
Tonsils
Should I have my child's tonsils removed?
Tonsiloliths
The throat (diagram)
The tongue and its associated bumps
Burning mouth/tongue syndrome (BMS)
Bald tongue (atrophic glossitis)
The floor of the mouth
The major and minor saliva glands
The facts about oral cancer (signs, symptoms and factors)
Leukoplakia and erythroplakia
Cancer of the lip
Tumors of the salivary glands
Malignant melanoma
Screening for oral cancer
Non cancerous lumps, bumps and abnormalities in the mouth
Tori and exostoses (hard bony tumors on the palate and gums)
Tongue abnormalities
Burning mouth/tongue syndrome (BMS)
Bald tongue (atrophic glossitis) (beefsteak tongue)
Lingual tonsils
Black or white hairy tongue
Geographic tongue
Enlarged Circumvallate papillae
Median Rhomboid Glossitis
Ankyloglossia (tongue tied)
Abnormalities of the gums
Gingivitis
Periodontitis
Trench Mouth (ANUG)
Pericoronitis
Parulus
Abnormalities of the lips and inside of the cheeks
Canker sores (aphthous)
Stenson's duct
Cold sores (herpes Labialis)
Angular cheilitis
Mucocele
Fordyce granules
Lichen Planus
Fibroma
Nicotinic Stomatitis (smokers palate)
Amalgam Tattoo
The oral manifestations of AIDS (HIV)


Have you ever wondered what that little thing that hangs down in the back of your throat is called? A glance at the diagram above will tell you it is called the Uvula. What's it for? It acts as a very effective valve that keeps food and drink from regurgitating up into the nasal cavity when eating or drinking (see diagram below). It vibrates while snoring, and when it is removed (usually in a procedure to reduce snoring) people seem to have minor problems immediately after the surgery with nasal regurgitation, especially when drinking carbonated beverages.

This problem goes away a few weeks after the surgery. The other structures, labeled clockwise around the diagram are as follows:

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The Labial Frenum is a little tag of tissue in the center of the upper and the lower lip that attaches the lip to the gums. It too is not especially useful, and sometimes causes orthodontic or periodontal problems if the attachment on the gums is too close to the teeth. If it becomes a problem, we usually simply cut it . This is most often done on children if the attachment of the frenum is too "high" and causes a diastema (space) between the adult teeth. The procedure is called a "frenectomy". An interesting thing to note is that a glancing blow to the face will generally rip this structure, and a ripped labial frenum, in combination with other "recurrent" bodily injuries is considered to be a legal indication of child abuse.


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The gingiva are what most people call the "gums". These are covered in more detail below.


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The roof of your mouth has two distinctive parts. The Hard Palate is the tough, leathery, non movable part of the roof of your mouth that is attached to the inside of your teeth and curves up to make the vault of your palate. The Soft Palate lies behind the hard palate and is closer to the back of your throat. You can feel the dividing line between the hard and soft palates with your tongue if you can draw it back that far. The Uvula is attached to the back of the soft palate. The Hamulii (singular hamulus) are hard little bumps in the corners of the soft palate just where the soft palate meets the very back of the tuberosities. If you press hard with the tip of the tongue to the inside and behind the gums behind the last top teeth, you may be able to feel them. They represent the tips of little projections from the base of your skull called the hamular processes of the palatine bone.


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The Maxillary Tuberosities are the tough, hard humps behind your top back teeth on both sides of the dental arch (note that both upper and lower teeth are arranged in "arches"). These humps have underlying bone and hard gum tissue covering them, and they are persistent, permanent parts of the mouth, even if all the upper teeth are extracted.


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Your Tonsils are at the border between your mouth and your throat. The Tonsils you can see at the corners of your throat are called the palatine tonsils. They are, in fact, only a part of a ring of tonsilar tissue that lines your entire throat. If you stick your tongue out really far, you can see some bumpy, pink (sometimes bluish) tissue toward the back on both sides. These are called the lingual tonsils. The lingual tonsils extend to the top (dorsal) surface of the tongue further back down your throat (see diagram below). Above the soft palate, about even with the palatine and lingual tonsils lie two similar masses of tissue called the Adenoids. These complete the tonsilar ring, so called because the palatine tonsils, lingual tonsils and adenoids form a complete ring of tonsilar tissue surrounding the throat. The tonsilar ring is composed of lymph nodes. Lymph nodes are a part of a separate "circulatory system" called the lymphatic system which acts like a drain to help keep the hydrostatic system of the body in balance. It keeps the various parts of your body from swelling up due to too much water pressure by allowing the water to redistribute itself. (In Tropical climates, the bite of certain mosquitoes can transfer a nasty little parasitic worm which lodges in the lymphatic system thereby blocking it and causing enormous swelling of various parts of the body. The condition is called "elephantiasis"--see image to the right) The lymph nodes (including the tonsils) act as a sort of filtration system to keep the fluids in the lymphatic vessels free of germs so that a localized infection does not spread to distant parts of the body through the lymphatic system.

Should I have my child's tonsils removed?
The thumbnail on the right (click on it to enlarge) shows typical palatine tonsils in a young child. (They shrink as we get older.) You can see that tonsils can take up quite a bit of room in the throat, and while they are not removed as casually today as they were earlier in the 20th century, their removal has certain advantages. They are a major factor in the constriction of the throat that causes snoring and obstructive sleep apnea, and when infected they can enlarge even more and add to the misery of a sore throat. When infected with Strep bacteria, numerous small yellowish-white plaques (white spots) appear all over them in the crevices (tonsilar crypts) that are visible over the surfaces of the tonsils seen in this image. These plaques are active colonies of the Streptococcus organism. Tonsils, like other lymph nodes, may enlarge during the course of viral and bacterial illnesses, and when this happens, constriction of the throat becomes more severe.

Of course the palatine tonsils do have physiological functions associated with the immune system. However they are fairly redundant (that is, there are a lot of other lymph nodes in the area which have the same function), and while some parents and politically inclined health organizations would sooner see their children lose their heads rather than their tonsils, no one ever seems to suffer any permanent adverse affects from their removal.

Conversely, their physical absence has a number of distinct advantages relating to less constriction of the airway and fewer complications from chronic infections. The major advantage of removing a child's tonsils is that the operation is much less painful for children than it is for full grown adults. If it becomes necessary to remove the tonsils during adulthood, the convalescence period is about two weeks of severe pain, especially upon swallowing. (Adults tend to lose a lot of weight. Children have fewer problems.)

Tonsiloliths (tonsil stones)

People with chronic sinusitis and post nasal drip may develop tonsiloliths, which are tiny, white, foul smelling stones which lodge in the tonsilar crypts. Sometimes a tonsolith can be pried out of the surface of the tonsil with a pencil or other small pointed instrument leaving what appears to be a little "hole" but is, in actuality, the tonsilar crypt in which it originally formed. Tonsiloliths sometimes give the feeling of something lodged in the throat. They can also contribute to bad breath. Some people have chronic problems with tonsiloliths. The only sure treatment for chronic tonsiloliths is removal of the tonsils. The operation is performed by an ear, nose and throat specialist (ENT) and is fairly simple and safe. As noted above, in adults the operation causes a very serious sore throat for two weeks post-op. Short of removing the tonsils, the bad breath can be treated with mouth rinses, and the condition itself may be lessened by gargling with Peridex® mouth wash which is available by prescription from your dentist or physician, and possibly by the use of decongestants to lessen the post nasal drip which is part of the cause of tonsiloliths.

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The Retromolar Pad is similar to the maxillary tuberosities discussed above, except that it is behind the last lower molars, and it is not underlain by a corresponding hump of bone. Even so, it, like the tuberosity, is a persistent landmark and remains as a hump of tissue even if the lower teeth have all been extracted.


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The Vestibule is the curvature of the tissue where the lining of the inside of the lips (labial mucosa) or cheeks (buccal mucosa) meet the gingiva (the gums). If you run your tongue around the outside of the teeth and extend it as far as it will go down (or up) into the cheeks keeping it in contact with the gums, the tip is extended into the labial or buccal vestibule.


Place the cursor over the image to identify the various anatomic structures

The image above shows the actual anatomy of the gingiva, known commonly as the "gums". The lighter pink colored gum tissue is called the "attached gingiva" because it is firmly attached to the underlying bone. It has the same consistency as the gums overlying the hard palate discussed above. The darker pink tissue above it is called the unattached gingiva also called the Alveolar Mucosa. It is not firmly attached to the underlying bone. The junction between them is called the mucogingival junction. The small margin of tissue outlined in yellow on the lower diagram is called the free or marginal gingiva (sometimes called the free gingival margin), and it is the unattached, sleevelike portion of the gingiva that encircles the tooth to form the gingival sulcus.

The Vermillion border is the junction of the dry, pink part of the lip with the skin of the face. The labial (lip) vestibule is marked on the diagram. The Upper Labial Frenum is also visible.
The Throat

The illustration on the right shows what is called a sagittal section of the face and neck. Note the proximity of the back of the tongue, the soft palate and the epiglottis to the back of the throat. The area between these structures and the back of the throat represents the narrowest parts of the airway and it is the narrowness of the airway in these areas that are of chief concern in the treatment of snoring and obstructive sleep apnea. The throat is a dual purpose organ allowing both the function of breathing and of eating and drinking. Air goes down the trachea to the lungs and food and drink go down the esophagus into the stomach. A remarkable little organ called the epiglottis is the valve that determines into which tube the air or food flows. This organ closes over the trachea blocking it off when anything but air is flowing through the throat. It opens when the person is breathing. You do have conscious control of the epiglottis. You can get a sense of where it is by clearing your throat. During this process, the epiglottis obstructs the trachea (airway) while you are exhaling, blowing air past the partially closed valve.

The Tongue (and its associated "bumps")


The tongue is composed entirely of muscle and connective tissue covered with two types of mucosa (Mucosa is the pink "skin" in the mouth). The image on the left shows part of the lingual tonsil on the lateral (side) surface. The lingual tonsil is much larger than the portion shown here. It curves up and around the posterior top surface of the tongue too (see the graphic below). The ventral surface is the underside of the tongue and it is smooth and not involved with tasting food. The dorsal surface is on top and is covered with a thin, pink velvet carpet. The velvet is composed of tiny hair-like projections called "filiform papillae".



The filiform papillae are a bit like hair in that they keep growing throughout your life. The image on the left is a false color electron micrograph of the filiform papillae on a cat's tongue. Human filiform papillae are similar except they tend to be flatter and lie down instead of sticking up in little points (see the image of fungiform papilla below). Click on the image to see a larger version. In healthy people, the individual hairs are shed before they get too long, and the natural red color of the underlying tongue tissue shows through giving the top surface of the tongue a velvety pink appearance. In some disease conditions (mostly fever causing diseases), the hair does not shed easily and forms a white, or sometimes even a black "coat" on the dorsal surface of the tongue. The filiform papillae are naturally white, but are often stained brown or black by foods or by dry mouth. When the filiform papillae grow too long, they remain on the dorsum of the tongue like a thick mat. This condition is known as "white hairy tongue" or "black hairy tongue" (see images below). A white or black coating on the tongue is NOT necessarily associated with any particular disease condition. This overgrowth of "hair" is easily removed by scraping the surface of the tongue with a tongue scraper. The filiform papillae are not associated with the sense of taste. White and black hairy tongue are not contagious conditions. Click on either image below to see larger versions.



The floor of the mouth

The image to the right shows the undersurface of the tongue. The thin strip of tissue that runs vertically from the floor of the mouth to the undersurface of the tongue is called the lingual frenum. It tends to limit the movement of the tongue, and in some people, it is so short that it actually interferes with speaking. It is a simple matter to "snip" this chord under local anesthesia. It is most often done when a child is between 5 and 9 years old. The procedure is called a lingual frenectomy.

The "V" shaped hump of tissue in the floor of the mouth houses a series of saliva gland ducts. The two largest ducts are in the center just in front of the attachment of the lingual frenum and are called Wharton's Ducts. They empty the submaxillary saliva glands (also known as the submandibular salivary glands). These ducts can be quite active in some persons, and upon occasion, a "fountain" of saliva may erupt from them while the patient is talking causing one of those embarrassing moments. The Sublingual saliva glands glands empty through a series of tiny ducts in the tissue on either side of Wharton's ducts.

If you look carefully at this image, you will note some blue tinted tissue under the tongue and in the floor of the mouth. These represent the presence of superficial veins that run in this area, and they are called varicosities. Their presence is normal, becoming more and more prominent as the patient ages.



If you look at the surface of your tongue, you will notice many tiny bumps scattered in among the velvet along the edges of the dorsal surface. The bumps are another type of papilla called "fungiform papillae" (named in honor of their mushroom-like shape). These are small, slightly raised and slightly redder than the surrounding "velvet" filiform covered surface that surrounds them. Foliate papillae are a third type located on both sides of the tongue in a small area just above (dorsal to) the lingual tonsils on the lateral surface of the tongue. The fungiform and foliate papillae are associated with taste buds. These papillae tend to be specialized with respect to the type of taste buds they contain. The image above and to the right shows the areas on the tongue which contain the fungiform and foliate papillae with taste buds specialized to taste the four basic tastes. (Our sense of smell is intimately linked to our sense of taste, and it is in our nose that we taste everything besides salty, sweet, bitter, and sour.) Notice that on this little image the back of the dorsal surface of the tongue contains a series of large bumps. If you stick out your tongue, you can see them on your tongue too. These large bumps on the top surface of the back of the tongue are a fourth type of papilla called circumvallate papillae. They are located along the "circumvallate line" and contain taste buds that confer the sense of sour and bitter to the back of the tongue. They can actually be quite prominent and are often mistaken by patients for cancerous growths.
No, this child does not have Blue Tongue Disease! (There is no such thing--in humans anyways. Such a disease does exist, but it only affects cattle, goats, sheep and deer.) A few drops of blue food coloring were applied to demonstrate the general size and location of the (otherwise pink) fungiform papillae which are the little bumps scattered all over the top surface of the tongue. They are usually difficult to see unless an overgrowth of filiform papillae causes the ordinarily pink velvet of the tongue to turn white, in which case the fungiform papillae stand out as red dots.
This is a micrograph of a fungiform papilla (the large round structure in the center of the image) surrounded by hairlike filiform papillae, which in this case are "combed" down and are lying side by side.

Macroglossia (large tongue)

The tongue normally resides on the inside of the arch formed by the lower teeth. Most people's tongues fit neatly into this space, however, a minority of people have tongues which are a bit larger than the space available. This does not mean that the patient cannot actually fit their tongue into this space. The tongue is a very flexible organ, and can accommodate itself to the prevailing conditions easily. On the other hand, once fitted into the space, it relaxes and presses up against the teeth. This causes the tongue to fill up the space available. Tongues like this have scalloped edges like the one pictured to the left. The scallops reflect the shape of the teeth as well as the spaces between them. This condition is sometimes associated with burning around the edges of the tongue. Click the image to see why, and for larger images.

Fissured tongue (scrotal tongue)

Fissured tongue, also known as scrotal tongue is characterized by folds and fissures in the dorsal (top) surface of the tongue. The fissures are of variable depth and usually extend laterally from a median groove as is pictured in the thumbnail to the right. This condition does not cause any symptoms, unless food particles and debris lodge in the depths of the fissures causing a mild glossitis (inflammation of the tongue). It is considered to be a normal form of tongue anatomy. Click on the thumbnail to see a larger version.



(Many people who inquire about "bumps on the tongue" are worried about HIV and AIDS. Please click on the icon to the right to view a complete explanation of AIDS and its oral manifestations.)




Burning mouth syndrome (BMS) (also known as burning tongue syndrome)

A small percentage of older men and women (mostly women), generally at, or around the age of menopause develop a problem with chronic burning pain and phantom tastes in their mouths. It often centers on the tongue. The tongue itself looks perfectly normal. It just develops a burning sensation that progresses throughout the day. These patients may have seen numerous doctors to try to rid themselves of the annoying, and sometimes painful symptoms, but generally to no avail. The problem has been ignored for centuries because there seemed to be no physical reason for the symptoms, and because it was believed that it was a hysterical symptom brought on by emotional distress. In fact, the problem sometimes does respond to antidepressant drugs like Elavil.

Recent research has revealed a hypothesis which might explain BMS (Burning Mouth Syndrome). It involves actual damage of the seventh cranial nerve which supplies the taste buds in the anterior 2/3 of the tongue. This may be caused by either (or perhaps both) the change in hormonal balance due to menopause and/or a viral infection. The theory is that these persons have lost much of their ability to taste, even though many do not realize their loss since the brain is good at amplifying small signals. The loss of the function of the 7th nerve leaves the trigeminal nerve (which allows the tongue and mouth to experience pain sensation) in a position of dominance. This theory assumes a sort of balance between the two nerves, and if a patient suffers a loss of ability to taste because of damage to the 7th cranial nerve, then the brain exaggerates the impulses from both the trigeminal and the 7th cranial nerve causing a constant burning sensation because of exaggerated trigeminal sensitivity. In addition, due to exaggeration of impulses from the 7th cranial nerve, the brain begins to generate phantom taste sensations. This sort of taste hallucination is similar to the tactile "fat lip" sensation that a patient feels when the conduction of the trigeminal nerve is blocked by a shot of a local anesthetic to numb the lower teeth.

Sometimes people develop this problem due to a hypersensitivity to some toothpaste or oral rinse that they have recently begun using. The first line of defense is to change your toothpaste to a type with only fluoride (Tom's of Maine is a reasonable choice) and cut out mouth rinses. The type of toothpaste most often involved with this type of hypersensitivity are those containing pyrophosphates which are added to reduce the buildup of calculus (like Crest Complete or Colgate Total) Also try to determine if you have recently been taking a new medication whose introduction coincided with the onset of the symptoms. A simple change of medication could make the difference.

It was discovered, quite by accident, that patients suffering from epilepsy who also suffered BMS experienced relief from the symptoms of both of these ailments by the administration of the epilepsy drugs clonazepam (Klonopin) and gabapentin (Neurontin). Thus a small, once or twice a day oral dose of of one of these drugs has been found to relieve the symptoms of BMS in most patients. Alternatively, clonazepam may be dissolved in the mouth using 1/2 of a .5 mgm tablet twice a day. Another drug which has been found to be useful in treating BMS is Chlordiazepoxide (Librium) not to exceed 10 mgm three times per day.

Another treatment that may work (or at least reduce the symptoms) in about 1/2 of sufferers is capsaicin desensitization. Capsaicin is the ingredient in hot peppers that makes them hot. The regimen is dilution of one part Tabasco sauce in two or three parts water with the patient rinsing and expectorating (spitting out). This is done every 2-3 hours at first, and tapering off over a day or two to once or twice a day. Be careful. Some people are hypersensitive to capsaicin, so if the burning is too severe, stop immediately!

Bald tongue (Atrophic glossitis)

As people begin to reach their senior years, sometimes they notice that their tongue begins to burn when eating sharp tasting foods. A look in the mirror reveals a beefy red tongue lacking the filiform papillae which, in health, give the top (dorsal) surface of the tongue a normal, light pink, velvet appearance. The loss of the filiform papillae is known as atrophic glossitis, and it may be caused by several different factors. Click on the image for a larger view.

The first factor is nutrition. Atrophic glossitis is most often caused by a lack of B vitamins in the diet. The addition of daily doses of folic acid, niacin, vitamin B12, pyroxidine, riboflavin, and even Iron, all in the form of a simple daily multiple vitamin tablet may help to restore the tongue and relieve the burning on eating.

The second factor is an oral yeast infection known as thrush, also known as candadiasis. In older patients with weak immune function, the mouth acts as a good incubator for yeast cells. These accumulate under a denture and often cover the tongue leaving a white coating that is easily scraped off revealing red tissue underneath. This is easily treated with Mycelex troches, or a single Diflucan tablet. Both of these are anti-fungal medications.

The third factor is mechanical abrasion of the tongue against a rough dental appliance, or occasionally on the teeth themselves, producing a more localized, persistent area of smooth surface on the tongue. This is treated by building a new denture and repairing or removing rough, broken teeth. Sometimes it is as easy as scraping hardened dental calculus off the insides of the lower front teeth.


The Saliva glands

There are three pairs of major saliva glands. The Parotid glands are on the sides of the jaw just below and in front of the ears. They are the "pickle glands" that create that funny feeling on the sides of your face when you first taste something really sour. The reason you feel it is that the parotids are contracting, expressing a sudden burst of saliva into the mouth. The glands empty through tiny holes in little bumps on the inside of the cheeks. These bumps are called Stenson's ducts and you can feel them with the tip of your tongue on the cheeks on either side of your mouth beside the upper back molars. The sublingual and submaxillary (also called the submandibular) glands empty into the mouth through ducts under the tongue. For a more detailed diagram and explanation of the anatomy of the major salivary glands, click here.

Sometimes one of the ducts to a gland will become blocked, generally due to a calcium deposit called a sialolith, or a salivary stone. When this happens, the patient may notice a transient swelling in the face that comes whenever he eats, or thinks about food. The swelling corresponds to the time when the salivary gland is producing saliva. The sialolith causes the saliva to back up in the duct or in the gland itself. Ordinarily, saliva always flows from the gland into the mouth, and this keeps germs from the mouth from progressing up the duct into the gland. But when the flow of saliva is blocked, bacteria can now enter the duct. Infections of this nature are called retrograde infections because the lack of flow of body fluid in the normal direction allows the germs to flow backwards (retro) into the organ that produces it. This problem is treated by an oral surgeon who clears the duct or removes the stone, and administers antibiotics.

There are also about 600-1,000 minor salivary glands, which occur just under the mucosa (pink skin) all over the inside of the mouth, except on the top surface of the tongue. They are located beneath the lining of the lips, the undersurface of the tongue, the floor of the mouth, the hard and soft palate, inside the cheeks, nose, sinuses, and the larynx (voice box). These glands are susceptible to retrograde infections and blockages of the duct just like the major salivary glands. When this happens, the patient may notice a small reddish (inflamed) lump or bump, sometimes sore, sometimes not. These small lesions can happen anywhere on the smooth pink mucosa lining the lips, cheeks or undersurface of the tongue and floor of the mouth, as well as on the hard palate. Duct blockages often cause the swelling to take place at or around mealtime. The swelling generally subsides between meals.


If you have come here to look for images of lumps, bumps, sores or discolorations that you noticed in the mirror this morning, there are three other pages with images you may find useful. Start on this page.

Then proceed to three other pages on which you will find more images of both normal and abnormal oral structures and lesions.

* Oral cancer
* Lumps, bumps and sores and discolorations
* Disease processes

The index on this page includes links to subjects covered on the cancer and lumps & bumps pages.




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tooth anatomy

The Crown

The crown of the tooth is that portion of the tooth that is covered with enamel. In most people, the crown lies nearly entirely exposed above the gum line. In children, the gingiva may partially cover the cervical (lower) part of the enamel.

Enamel

Enamel is the substance that covers the crown of the tooth. It is very hard and quite resistant to mechanical and chemical attack. Its purpose, of course, is to protect the tooth from the dangers posed to the teeth by the oral enviornment. In general, it is vulnerable only to acid attack from excess sugar (decay), generalized trauma such as a blow from a hard object, and serious bruxing with associated attrition. It is white, but somewhat translucent and allows the color of the underlying dentin to shine through to a certain extent which is why teeth look yellow. In the diagram to the left, the enamel is represented by the top layer on the tooth. Here it looks a bit like a neat haircut. The reason it is drawn that way is because the enamel is made up of microscopic enamel rods all of which run about parallel to each other and which project perpendicularly from the surface of the underlying dentin. When you are looking at a tooth in the mouth, you are seeing millions of these little enamel rods packed side by side, but you are seeing them end-on, as in the illustration on the right which is a reasonable representation of their cross section. They are packed together a bit like an Escher drawing.



The micrograph above on the left shows the rods in sagittal section, which means you are seeing them as if the tooth were cut like the tooth in the "haircut" image above. The image on the right shows the enamel rods end-on after etching the surface with acid. The acid treatment dissolves the internal parts of the enamel structure faster than the outer parts, so you are seeing only the outline of the rods. The actual rods are solid structures, but do not show up well in micrographs.

Each enamel rod is attached to the dentin underneath it. For this reason, cracks in the enamel (crazes) penetrate only as far as the dentin. This method of attachment makes it impossible for the enamel to separate from the tooth no matter how many crazes develop in its structure.

Dentin



Dentin is the hard, yellow bone-like material that underlies the enamel and surrounds the entire nerve. It composes the bulk of the tooth, and is sensitive to touch and other stimuli. In the image at the top of this page, the illustration shows thousands of tiny little lines that run approximately parallel to each other and perpendicular to the surface of the nerve space. These lines represent tiny tubes that run parallel to one another throughout the structure of the dentin. These are called dentinal tubules, and they originate from the inner surface of the nerve space and travel perpendicularly from their point of origin to the surface of the tooth terminating at the undersurface of the enamel, or the surface of the root itself in areas where it is not covered with enamel.

The tubules contain tiny projections of cells that line the inside of the nerve space. These cells are called odontoblasts, and they are actually the covering layer of the nerve itself. The projections of the odontoblasts into the dentinal tubules are not nerves. However, the odontoblasts connect with nerve axons in the dental pulp (nerve). Exposed dentin is sensitive to touch, air and other stimuli because these stimuli cause movement of the fluid in the odontoblast projections inside the tubules. This movement of fluid can be sensed by nerve endings in the dental pulp which anastomose (connect) with the odontoblasts. The image on the right above is an electron micrograph of actual dentinal tubules seen end-on.

The dental pulp (the nerve of the tooth)

What the lay public calls the nerve of a tooth is called the dental pulp by dentists. It is a complex organ composed of connective tissue, blood vessels, and nerve axons. It is pink and soft, and looks just like the lining of the mouth when it is removed during root canal procedures. Its original purpose during development is the formation the teeth themselves. In other words, the nerve of a tooth is a "generative" organ. The nerve starts out as a clump of specialized cells, and as we begin to grow, it slowly takes the shape of a tooth. The cells on the outside of the pulp begin to form the various hard structures , enamel and dentin, that we associate with the tooth itself. The tooth is formed from the outside toward the inside, with the dental pulp slowly replacing itself with tooth structure. While we are still young, the nerves in our teeth are relatively large, but they slowly shrink becoming more and more narrow throughout our lives. Once the tooth is fully formed, the nerve slows its formative functions, but it keeps building dentin in a process called dentinogenesis. During this slow growth phase of its life, the nerve serves mostly to keep the teeth hydrated and allows the dentin to retain a certain amount of elasticity. Thus, living dentin acts something like a shock absorber, preventing the teeth from fracturing. Whenever a nerve in a tooth dies, the tooth looses this shock absorber effect and is more prone to fracture. This is the reason that a tooth that has been endodonticly treated needs to be protected with a crown.

Root canals (endodontic treatment of the dental pulp)

A "root canal" is actually only a part of the dental pulp. It has all the same characteristics and functions as the rest of the dental pulp, except that it is located inside the root portion of the tooth and is thus rather thin and spindly. When we tell a patient that they need a "root canal", we are not talking about the anatomical structure itself. We are talking about a procedure. We really mean that the nerve is sick and must be removed in its entirety from the tooth, the empty space where it used to live cleaned and sterilized and finally sealed with a form of rubber called gutta percha or one of the newer materials designed for this purpose. The technical name for this procedure is "endodontic treatment". The root canal(s) in any given tooth start out just like the rest of the nerve, as a solid piece of soft tissue. Blood vessels and nerves enter through a hole at the tip of each root. The tip of the root is called the "apex", and the hole that allows the nerve tissue, with its accompanying blood vessels to enter the tooth is called the apical foramen. Of course, blood must traverse through the root canals in order to infuse the nerve. As we age, the root canals too replace themselves with more and more dentin until they become less tube like and more like a network of blood vessels and nerves running down approximately the center of the root. The image to the right shows some of the complex anatomy that the dentist is presented with when he must perform a root canal procedure to relieve pain and infection. In fact, the nerve anatomy can become even more complex as we age. As the canal becomes thinner and thinner, we say that it has become sclerosed. One can see that it could be quite difficult to remove ALL the dead tissue in the root canals if its internal anatomy has become more and more sclerosed and difficult to negotiate as the tooth ages or becomes sick. While it is important for the endodontist to remove as much dead nerve tissue as possible from the pulp chamber and root canals, the final line of defense against endodontic failure is to make sure that any remaining dead nerve tissue inside the tooth is properly sealed off at the apical foramen and any other openings in the root by properly fitted and placed sealing materials.

The cementum

Cementum is to the root of a tooth as enamel is to the crown. Cementum is a relatively soft bony tissue that covers the root surface in a thin layer. Its main function is to act as an attachment layer for the periodontal ligament which is a soft tissue sheath that acts as a cushion between the bony socket and the tooth itself. It is relatively soft and does not wear well against environmental assaults, so it abrades away rapidly whenever it is exposed to the oral environment because of recession. The image to the right shows the relationship of the enamel that covers the crown of a tooth, to the cementum that covers the root. Unless there is wear of the cementum due to recession, or attrition of the enamel due to bruxing or mechanical abrasion, the dentin is never exposed. The cementum meets the enamel in a line that surrounds the tooth. This line is called the cemento-enamel junction.

The apical foramen

The apical foramen is simply the hole in the tip of the root where the nerve and all its accompanying blood vessels must enter the tooth. Each root has a foramen at its tip and blood must both enter and exit the dental pulp from this point. The foramen is often not located at the very tip of the root, but may be offset one to three millimeters toward the crown of the tooth.

tooth anatomy

Note: This page is written for students planning a career medicine or in one of the dental fields. It contains more technical information than most people in the general public want to know. Click on the icon at the right to see a labeled diagram and text without the confusing terms.



The structures that support the teeth

Healthy teeth are, of course, embedded in bone. The bone is covered with gums, and the gums attach not only to the bone, but also to the tooth itself.


The gingiva

The gingiva is that portion of the gums that surrounds the teeth and lies above the level of the bone. The diagram to the right is a detail which shows the microscopic structure of this vital attachment of the gums to the tooth. The soft tissue is covered by an epithelial layer (red) called the oral epithelium. This attaches to the surface of the tooth on the dentin between one and three millimeters below the level of the crest of the gingiva. The part of the gingiva below the crest but above the attachment is called the free gingival margin. The potential space between the free gingival margin and the tooth (collapsed in life) is called the gingival sulcus. Just below the epithelial attachment lies a large number of connective tissue fibers (blue) called the gingivo-dental fibers. Some, which are not visible here actually circle the entire tooth and are called circular fibers. These fibers are responsible for securely attaching the gingiva to the tooth.

This attachment is responsible for separating the dirty oral environment from the totally clean environment inside the body. The gingival attachment is doubly important because it protects the underlying bone (alveolar crest) from becoming infected. Nature is especially protective of the bone because it is not highly vascularized and an infection in bone, especially in pre modern man's environment would have been a death-dealing event. An infection in bone is called osteomyelitis, and even today, with modern antibiotics, it is still quite a dangerous condition. Thus nature built in a simple mechanism to protect mammals from getting osteomyelitis as they aged and became more susceptible to oral infection. She programmed the bone to resorb (to be absorbed); to "get out of the way" before the infection reached it. This is the basis of periodontal disease---The loss of bone as a protective mechanism against a dangerous bone infection. Better the loss of the teeth than the premature loss of life!

The periodontal Ligament (PDL)

The periodontal ligament is just visible in the diagram immediately above. It is the soft tissue that lies between the tooth and its bony socket. As you can see, it is really just a continuation of the connective tissue associated with the gingivo-dental fibers, and if you look at the large diagram at the top of the page, you can see that it continues around the entire tooth. In a healthy situation, there is never a direct attachment between the bone and the tooth itself. Such a direct attachment, when it occurs in pathological situations, is called ankylosis.

The PDL is composed of fiberous connective tissue in which the fibers run approximately perpendicularly from the tooth surface to the bony socket. In any given area, a cross section looks like a tangled mass of nearly parallel fibers that attach at one end into the cementum overlying the root of the tooth, and at the other end, into the aveolar bone inside the socket.



The bone that supports the teeth is called alveolar bone. It's only purpose in life is to support the teeth, and if a tooth is extracted, the alveolar bone that originally supported it will eventually be resorbed by the body. The part of the alveolar bone that lines the socket is a thin layer of dense cortical bone called the lamina dura. The bone that underlies the lamina dura is cancellous bone (sometimes called medulary bone). Cancellous bone looks spongy and contains blood producing "organ" called bone marrow. In fact, all three of the features discussed in this section, the lamina dura, the periodontal ligament and the cancellous bone can be seen on any intraoral dental x-ray. In the x-ray seen on the left, follow the edge of any of the three teeth present from the top of the crown down into the bone. The dark line that separates the tooth from the bone represents the space where the periodontal ligament lives. The thin bright strip of bone directly beside the periodontal ligament space is the lamina dura. Under the lamina dura is the less bright cancellous bone. If you look carefully you can see the trabeculii --the tiny spicules of bone crisscrossing the cancellous bone that make it look spongy. These trabeculii separate the cancellous bone into tiny compartments which contain the blood producing marrow. These marrow spaces are seen in the colored image of the PDL above as bright "blobs".

reimplanted tooth

What if you or your child knocks out a front tooth?

Step by step instructions for patients and for dentists



The accidental loss of an adult tooth is a grave event and very tricky to treat. Even the best techniques sometimes fail to permanently save the tooth. As you read the rest of this page, bear in mind that there is a distinct possibility that you or your child may loose the tooth even though every step is religiously followed!

Instructions for the patient

Procedures for the dentist

If patient presents with tooth already reimplanted in socket

If patient presents with tooth in hand or improperly reimplanted

If tooth has open apex (blunderbuss)

If tooth has fully formed root (apex)

Splinting the tooth in position

Managing the tooth after the reimplantation


Instructions for the accident victim or parent

1. If the tooth is one of the four front baby teeth (deciduous teeth), there is NO NEED to reimplant it (ie do not replace it in the socket). Front baby teeth do not hold space for the adult teeth that will begin to erupt at age six, and the early loss of one of these teeth rarely causes harm to the adult dentition.

2. If the root of an adult tooth is broken, (especially if part of the root remains in the socket) reimplantation is not possible. Any attempt will fail. This means that the trip to the dentist, though necessary, may be put off until it is convenient. The only things a dentist can do under such circumstances it to prescribe antibiotics, and to place artificial bone in the socket for possible implant placement at a later date. The placement of artificial bone is a bit involved for an off hours emergency. The placement of artificial bone is generally best done under the auspices of an oral surgeon or a periodontist. These specialists have become the de-facto implantology specialists.

3. Any avulsed tooth must be reimplanted in the socket within 60 minutes if the reimplantation is to have a reasonable chance of working.

This may be done at the site of the accident by any adult including the patient himself provided the tooth is fairly clean and provided it slips back into the socket easily with light finger pressure. If the tooth goes back into its proper position so that the patient may bite down without pushing the tooth out of its normal alignment, then the process has been successful.

If the tooth is dirty, simply have the patient remove all dirt with their own saliva. Have the patient suck fairly hard on the tooth. Be sure that the patient spits out blood and debris after each sucking action. This removes dirt and will hopefully dislodge any clot that may have formed in the socket making it easier to reimplant the tooth.

You still must take the patient to a dentist, but the major emergency has been averted and there is less urgency associated with the emergency.

If the tooth cannot be replaced in the socket (for any reason), then there are three ways to transport the tooth to the dentist's office:

Have the patient remove dirt and debris by sucking on the tooth as above and then have the patient store the tooth in their own mouth in the pouch between the cheek and the top back teeth. Transport the patient to a dentist ASAP.

This is NOT advisable if the child is under the age of six since the child may swallow the tooth. If this is the case, proceed to the next two options.

Place the tooth is a cup of clean saline (salt water). You may make saline by placing one and a half teaspoons of salt in four cups of clean water. Tap water is acceptable, but bottled water may be cleaner if it is IMMEDIATELY available. The saline has the advantage of acting to clean off the tooth. Transport the tooth and patient to the dentist ASAP.

Place the tooth in a cup of fresh milk (any fat content). This has nearly the same advantages as saline. Transport the tooth and the patient to the dentist ASAP.

A commercial product is available for the storage of an avulsed tooth if you, or someone you know happens to have it in their medicine cabinet. The manufacturer states that the tooth may be reimplanted up to 24 hours after the avulsion if it is kept in this solution. It is called Save-A-Tooth, and can be ordered by clicking here.

Instructions for the dentist

1. If the tooth has been properly replaced in the socket at the site of the accident:

Do not extract the tooth to treat the root.

Clean the effected area with water spray, or chlorhexidine mouth rinse.

Verify proper alignment of the tooth by the following methods:

Have the patient bite down and verify that the tooth is not in traumatic occlusion and remains in acceptable alignment with neighboring teeth.

Take a periapical x-ray

if the tooth is in traumatic occlusion, remove the tooth from the socket and proceed to step 2 below.

Suture gingival lacerations

Splint the tooth with (preferably) a flexible splint. Have the patient bite into occlusion to eliminate traumatic bite prior to splinting. The splint will be kept on the tooth for 7 to 10 days.

prescribe a suitable antibiotic (doxycycline is ideal).

Refer to physician for evaluation of tetanus immunization.

If the tooth has an open apex (blunderbuss) avoid doing a root canal unless an abscess develops or there is radiographic evidence of pulpal necrosis.

Proceed to the Post-emergency procedures.

2. If the tooth has not been replaced in the socket, or if it must be removed due to traumatic occlusion or misalignment:

If the tooth has an open apex (not fully formed root)

If the tooth has been out of its socket for much more than an hour, or especially, if the tooth has dried out during transportation, the reimplantation procedure is unlikely to be successful, and the patient or parents should be so informed. It is still permissible to attempt reimplantation since survival is always possible, even if unlikely. It is, however unlikely that the root will continue to form its apex and apexification will be necessary. There is also a very substantial chance that the root will experience external resorption or become ankylosed. The most reasonable course of action is to warn the parents of this outcome and to avoid the procedure altogether.

If the tooth has been out of its socket for an hour or less, and has been properly transported to the dental office, then the procedure has a better chance of working. This implies that the blunderbuss root will continue to form an apex and the tooth will continue to erupt normally after the reimplantation procedure.

Clean the effected tooth with water spray or saline.

Place the tooth in a solution of doxycycliine if available (Low concentration, about 1mgm per 20 cc of saline. Can be made on premises using 1/2 of a 100 mgm tablet finely crushed and added to about a liter of saline. In most situations, this step is not especially practical and may be omitted if it is not possible. At minimum, clean the tooth with copious saline solution. Do not use antiseptic solutions on tooth.

Irrigate the socket with saline and remove all coagulum.

Inspect the socket. If bone is displaced into the socket, move it back into position with a suitable instrument in order to allow proper insertion of the tooth.

Replace the tooth in the socket with minimal digital pressure.

Suture gingival lacerations.

Take a periapical x-ray to check root alignment.

Splint tooth in position with (preferably) a flexible splint. Have patient bite into occlusion to be certain that the position is correct before applying the splint. The splint will be kept in place for about one week.

Prescribe a suitable antibiotic (doxycycline is ideal).

Refer to physician for evaluation of tetanus immunization.

Do not perform a root canal procedure unless a post op x-ray shows serious periapical involvement. The idea here is to allow the root apex to form normally. If the pulp dies at any point during treatment, then a root canal procedure with apexification will be necessary.



If the tooth has a fully formed root (apex)

If the tooth has been out of its socket for an hour or less, and it has been properly handled (as stated above in instructions for patients), the reimplantation procedure is the same as that shown above with the exception of the use of doxycycline rinse. The instructions are repeated below for clarity and completeness:

Clean the effected tooth with water spray or saline.

Clean the tooth with copious saline solution. Do not use antiseptic solutions on tooth.

Irrigate the socket with saline and remove all coagulum.

Inspect the socket. If bone is displaced into the socket, move it back into position with a suitable instrument in order to allow proper insertion of the tooth.

Replace the tooth in the socket with minimal digital pressure.

Suture gingival lacerations.

Take a periapical x-ray to check root alignment.

Splint tooth in position with (preferably) a flexible splint. Have patient bite into occlusion to be certain that the position is correct before applying the splint. The splint will be kept in place for about one week.

Prescribe a suitable antibiotic (doxycycline is ideal).

Refer to physician for evaluation for tetanus immunization.

Proceed to post-emergency procedures.

If the tooth has been out of the socket for well over an hour, or if the tooth has been allowed to dry out during transport, the treatment differs from that above mostly because of changes that have taken place on the surface of the root. The following procedure is designed to minimize external root resorption during post operative healing.

Rinse off all debris from the tooth with copious water or saline.

Gently and quickly root plane the root of the tooth to remove necrotic periodontal ligament and any foreign debris that has dried onto the surface.

Immerse the tooth in a 2.4% Sodium Fluoride solution acidulated to pH 5.5 for 5 minutes. This item is rarely found in dental offices today. It has been replaced with various neutralized rinses, gels and foams of lesser concentration. In the absence of the stronger solution, a lesser concentration of fluoride may be used instead. The idea is to convert surface hydroxyapatite into fluoroapetite to reduce external resorption during healing. Keep the tooth in the fluoride solution for a minimum of five minutes; 20 minutes if possible. Wash off the fluoride solution afterwards with copious saline. Click here to see a clinical study recommending this procedure.

Irrigate the socket with saline and remove all coagulum.

Inspect the socket. If bone is displaced into the socket, move it back into position with a suitable instrument in order to allow proper insertion of the tooth.

If available, apply Emodogain® to the inside of the socket. This is a specialty item and is not likely to be found in the offices of most general dentists. It has been found to be helpful in experimental situations but no human studies have been carried out to prove its usefulness in reimplantation of avulsed teeth. If available, it may be useful, but certainly not essential.

Replace the tooth in the socket with minimal digital pressure.

Suture gingival lacerations.

Take a periapical x-ray to check root alignment.

Splint tooth in position with (preferably) a flexible splint. Have patient bite into occlusion to be certain that the position is correct before applying the splint. The splint will be kept in place for about one week.

Prescribe a suitable antibiotic (doxycycline is ideal).

Refer to physician for evaluation of tetanus immunization.

Proceed to post-emergency iprocedures.

3. Spilinting the tooth in position:

The ideal splint for avulsed teeth is a flexible splint. These are typically made using Gortex or other synthetic cloth or metallic mesh strips made for this purpose. Other types of flexible splint may involve bonded orthodontic brackets and thin orthodontic wire. Ideally, the splint should encompass several teeth on either side of the avulsed tooth. There are quite a few options depending on the comfort level of the practitioner. The recommendation for flexiblity involves theoretical considerations in the formation of the new periodontal ligament. However, since the splint is kept in place for no more than 7 to 10 days, the flexibility factor may be of little practical significance. This is my personal opinion. I'm sure others would argue the point vehemently.

The simplest type of splint involves nothing more than a fairly thick strip of light cured composite running across three teeth with the avulsed tooth in the middle. I have found that this works quite well. The procedure for upper incisors (the most commonly avulsed teeth) involves having the patient bite into occlusion and keeping his teeth in this position for the entire procedure. This stabilizes the tooth and guarantees that the tooth will not be in traumatic occlusion. The three teeth are pumiced and acid etched. Bond is applied and light cured. Finally a fairly thick layer of composite is layered over the buccal surfaces of three teeth. I try to keep it neat, but this is a functional repair and will be removed in a week, so I generally use a color that contrasts with the teeth in order to make removal easier. I do not spend much time forming it to look like a restoration.

In the case of lower incisors, I place the splint on the buccal surface if the occlusion permits. Otherwise, I place it lingually.

The splint is removed in about a week (10 days tops) and assessed for mobility. If the mobility is excessive, then reapply the splint for another several weeks. Otherwise, allow the tooth to function normally.

4. Post-emergency procedures (managing the tooth after reimplantation):

Root canal procedure should be initiated in 7-10 days unless the avulsed tooth has an open apex and the tooth was reimplanted under optimal conditions.

The splint should be removed in 7 to 10 days unless the radiograph shows serious bony involvement along the lateral edges of the root.

If the tooth has a closed apex, or if a tooth with an open apex has obviously abscessed or shown radiographic evidence of pulpal necrosis, begin the root canal procedure prior to removing the splint.

At this time, instrument the canal completely and place calcium hydroxide paste in the canal. Allow the paste to remain in the canal for approximately a month prior to obturation of the canal.

The root canal procedure may be completed when an intact lamina dura can be traced all the way around the root. In most cases this will happen within a month. If the lamina dura has not begun to form, or if external resorption is apparent on the radiograph, then the calcium hydroxide should remain in the canal. The status of the lamina dura should be checked one month post op and at three month intervals after that. At the time of the exam, the calcium hydroxide paste should be washed out and replaced with fresh paste.