WHO 2017 Classification of tumours of Salivary Glands

Anatomy of Temporomandibular Joint (TMJ)

"Temporomandibular joint forms the craniomandibular articulation"

·  Two synovial joints (right and left) connected with a single bone “the Mandible” makes the joint unique. Further coordinated movements of both joints facilitates the mandibular movements.

·         Boney components

1.      Contyle of mandible

2.      Squamous temporal bone of the skull

·         TMJ is a Complex joint – by function and by structure

·         Also it is a “Ginglymoarthoridal” jt

                                    Hinging movement – Ginglymoid movement

                                    Gliding movement – Arthroidal movement

·         Another classification of joints classify TMJ as a Compound Jt

-          By definition compound jt is joint composed of 3 or more bones

-    TMJ is composed of 2 bones , but considered compound jt  because articular discis is considered functionally non ossified bone

-         TMJ differs from other diarthoidal joints of the body

  I.  TMJ forms bilateral diarthrosis – functioning both Lt  Rt joints together

 II.Articular surfaces are covered by fibrocartilage instend of hyaline cartilage

III.TMJ is the only joint which has argitend point of closure, because when the mouth is closed the teeth come into occlusal contact

The Disc

·         Dense fibrous tissue

·         Devoid of blood vessels and nerves. Therefore it does not manifest marked inflammation in trauma.

·         Four Regions

1.       Anterior

2.       Intermediated – sits along articular eminence

3.       Posterior – Thickest – 12 ‘o clock on contyle

4.       Bilaminar region (Contains Blood vessels)

Collagen type I – Mainly

1.       Superficial layers – Parallel to anterior-posterior direction

2.       Central – Oriented random fashion

This arrangement provide ability with stand forces

 

Structure of Temporomandibluar joint

Anteriorly Disc divides into two lamellae

1.       Superior Lamella – Fuse with capsule  the periosteum of the anterior slope of articular eminence

2.       Inferior Lamella – anterior surface of the neck of the condyle

3.       Mid – with fibers of lateral pterygoid muscle

Muscles of Mastication

Although they are called muscles of mastication, they always function with other groups of the face, tongue, soft palate & hyoid bone

Masseter                                        

Superficial Part

Arises from lower border of Zygomatic arch                                                                           

Fibers directed downward back wards

Insert along the angle of the mandible

Insertion-  Lower 1/3 of the posterior border of the ramus and along lower boarder of the mandible to the 8 tooth

Deep Part                                                    

           Inserts above superficial masseter along the ramus of the mandible                              -

Function

1.       Elevation of the mandible

Nerve Supple

                      V Nerve      >    Mandibular branch          >       Masseteric Nerve

                                              

Temporalis

-                                                        Fan shaped muscle

-                                                        Attachment of large muscle extend to 

                                 I.                     Small portion of parietal bon- extends above

                               II.                    Greater Portion of the savamous portion of the temporal bone

                             III.                    Temporal surface of the frontal bove

                             IV.                    Temporal surface of greater wing of the sphenoid bove

                                                                      

·         Temporal Fascia attaches to supra temporal in border of the zygomatic arch.

·         Temporal Fascia

o   Thickens When passing downwards.

o   Splits in to two layers.

o   Superficial layer blends periosteum of the lateral Surface of the Zygomatic arch.

o   Deep Portion blunts T medial Surface.

o   Many of the muscle fibers original from the medial surface of the temporal fascia.

·         Insertion of temporalis.

o   Coronoid   Process

o   Antero medial Surface of the ramus of the mandible.

·         Function

o   Elevates the mandible.

·         Innervation

o   Deep temporal branches arising from the mandibular division of   V

Medial Pterygoid

                2. Heads 

• Superficial Head
• Deep head

Deep head- Originates from medial Surface of lateral Pterygoid plate a Pyarmydal Process of the Palatine bone.

Inserted in to Roughened medial  Surface of the mandible near the angle of the mandible.

Superficial Head-Originals from Tuberosity of the maxilla adjacent Pyramidal process of the Palatine bone.

Joins with deep head to in sear in to mandible.

Runs-  Downwards

         -  Backwards

         -  Laterally

Innervated by – Nerve to medial Pterygoid.

                       _ Branch of the mandibular.

                       _ Division of the Trigeminal Nerve.

Lateral Pterygoid

Two heads

·         Superior head

·         Inferior head

v  Superior head – Originals from infra temporal Surface of the grater wing of sphenoid.

Runs backwards, laterally, almost horizontally and insert to the disk capsule of the TMJ the condyle.

Function – Stabilizer the mandibular condyle against the reticular eminence during mastication.

v  Inferior head - Originals from lateral Surface of lateral Pterygoid plate.

Fibers extend Back wads, Upwads Out wads to insert in to neck of the condyle.

Function

Protrusion

Lateral excursion

Innervation

Branch of buccal nerve- From mandible division of  V

Other muscles

1.       Digastrics

2.       Mylohyoid

3.       Geniohyoid

4.       Platysma

Vitamin D-What, Where, When, How, Why?

Vitamins are not generally considered to be endocrine substance, but it is a organic dietary factors essential for healthy life. The term ‘ vitamin D ’ refers to two steroid like chemicals, namely ergocalciferol and cholecalciferol . Vitamin D is important for good health, growth and strong bones and may also help to prevent other diseases such as cancer, diabetes and heart disease. A lack of vitamin D is very common. Vitamin D is mostly made in the skin by exposure to sunlight.  A mild lack of vitamin D may not cause symptoms but can cause generalised aches and pains and tiredness. A more severe lack can cause serious problems such as rickets (in children) and osteomalacia (in adults), described below. Treatment is with vitamin D supplements. Some people are more at risk of vitamin D deficiency, and so are recommended to take vitamin D supplements routinely. These include all pregnant women, breast-fed babies, children under 5, and people aged 65 and over. Also, people who do not get much exposure to the sun, people with black or Asian skin types, people who do not go out in the sun and people with certain gut, liver or kidney diseases.  We have checked our own patients and found that 9/10 adults of South Asian origin are vitamin D deficient and something like 60% of our white patients are vitamin D deficient.  Most people present with aches and pains and tiredness.

What is vitamin D?

Vitamins are a group of chemicals that are needed by the body for good health. Foods that contain vitamin D include the following though many foods do not contain much vitamin D and exposure to the sun is a better source of vitamin D than foods. Vitamin D is a fat-soluble vitamin. Most foods contain very little vitamin D naturally , though some are fortified (enriched) with added vitamin D.  Foods that contain vitamin D include:

                -Oily fish (such as sardines, pilchards, herring, trout, tuna, salmon and mackerel).

                -Egg yolk.

                -Fortified foods (this means they have vitamin D added to them) such as margarine, some cereals, infant formula milk.

Action of Vitamin D

The 1,25 - (OH)2 -D 3 receptor belongs to a superfamily of nuclear hormone receptors, which bind to their ligand and alter transcription. The hormone travels in the bloodstream in equilibrium between bound and free forms. The latter form is freely able to enter cells, due to its lipophilic nature. The plasma 1,25 - (OH) 2 - D 3 - binding protein (DBP) recognizes the hormone specifi cally. 1,25 - (OH) 2 - D 3 binds to the nuclear receptor; the complex binds to specifi c hormone response elements on the target gene upstream of transcriptional activation sites, and new mRNA and protein synthesis result.

New proteins synthesized include osteocalcin, an important bone protein whose synthesis is suppressed by glucocorticoids. In the GIT, a calcium - binding transport protein (CaBP) is synthesized in response to the hormone – receptor activation of the genome.

Physiological actions of vitamin D

Bone-Vitamin D stimulates resorption of calcium from bone as part of its function to maintain adequate circulating concentrations of the ion. It also stimulates osteocalcin synthesis.

Gastrointestinal tract-1,25 - (OH) 2 - D 3 stimulates calcium and phosphate absorption from the gut through an active transport process. The hormone promotes the synthesis of calcium transport by enhancing synthesis of the cytosolic calcium – binding protein CaBP, which transports calcium from the mucosal to the serosal cells of the gut.

Kidney- 1,25 - (OH) 2 - D 3 may stimulate reabsorption of calcium into the tubule cells while promoting the excretion of phosphate. The tubule cells do possess receptors for vitamin D and CaBP.

Muscle-Muscle cells have vitamin D receptors, and the hormone may mediate muscle contraction through effects on the calcium fl uxes, and on consequent adenosine triphosphate (ATP) synthesis.

Pregnancy-During pregnancy, there is increased calcium absorption from the GIT, and elevated circulating concentrations of 1,25 - (OH) 2 - D 3 , DBP, calcitonin and PTH. During the last 6 months prior to birth, calcium and phosphorus accumulate in the fetus. The placenta synthesizes 1,25 - (OH) 2 - D 3 , as does the fetal kidney and bone. Nevertheless, the fetus still requires maternal vitamin D.

Other roles- Vitamin D may be involved in the maturation and proliferation of cells of the immune system, for example of the haematopoietic stem cells, and in the function of mature B and T cells.

Our main source of vitamin D is that made by our own bodies. 90% of our vitamin D is made in the skin with the help of sunlight.

Ultraviolet B (UVB) sunlight rays convert cholesterol in the skin into vitamin D. Darker skins need more sun to get the same amount of vitamin D as a fair-skinned person. The sunlight needed has to fall directly on to bare skin (through a window is not enough). 2-3 exposures of sunlight per week in the summer months (April to September) are enough to achieve healthy vitamin D levels that last through the year. Each episode should be 20-30 minutes to bare arms and face. This is not the same as suntanning; the skin simply needs to be exposed to sunlight.

So, vitamin D is really important for strong bones. In addition, vitamin D seems to be important for muscles and general health. Scientists have also found that vitamin D may also help to prevent other diseases such as cancer, diabetes and heart disease.

Who gets vitamin D deficiency?

Vitamin D deficiency means that there is not enough vitamin D in the body. Broadly speaking, this can occur in three situations:

1. Increased need for vitamin D

Growing children, pregnant women, and breast-feeding women.

2. Situations where the body is unable to make enough vitamin D

People who get very little sunlight on their skin are also at risk of vitamin D deficiency. This is more of a problem in the most northern parts of the world where there is less sun. In particular:

                 People who stay inside a lot or cover up when outside or use strict sunscreen

                 People with pigmented (dark coloured) skins and elderly people  

                 Some medical conditions can affect the way the body handles vitamin D.

                     People with Crohn's disease, coeliac disease, and some types of liver                                                     and kidney disease, are all at risk of vitamin D deficiency.

                 Vitamin D deficiency can also occur in people taking certain medicines -                                                  examples include: Carbamazepine, Phenytoin, prim done, barbiturates and some anti-HIV                    medicines

3. Not enough dietary vitamin D

Vitamin D deficiency is more likely to occur in people who follow a strict vegetarian or vegan diet, or a non-fish-eating diet.

How common is vitamin D deficiency?

It is very common. This is why we recommend a regular supplement to our patients.  A recent survey in the UK showed that more than half of the adult population in the UK had low vitamin D. This level is found to be greater in people who have dark skin.  In the winter and spring about 1 in 6 people has a severe deficiency. It is estimated that about 9 in 10 adults of South Asian origin may be vitamin D-deficient. Most affected people either don't have any symptoms, or have vague aches and pains, and are unaware of the problem.  80% of our Asian patients have been found to be deficient and 60% of our white patients have found to be deficient.

What are the symptoms of vitamin D deficiency?

Symptoms of vitamin D deficiency are tiredness or general aches.  Because symptoms of vitamin D deficiency are often very vague, the problem is often missed.

How is vitamin D deficiency diagnosed?

Vitamin D deficiency can be diagnosed by a blood test.  However, on balance if you have dark skin and live in the UK you should take supplements. It may be suspected from your medical history, symptoms, or lifestyle. A simple blood test for vitamin D level can make the diagnosis.

RECOMMENDATIONS – Your doctor will advise you if you have deficiency or insufficient vitamin D.  If you have a minor level of vitamin D deficiency we recommend patients buy vitamin D tablets equivalent to 10ug or 12.5ug.  Most are made from vegetables.   If you have been found to be deficient we would recommend you stay on this dose for life as treatment is often needed long-term because the cause of the deficiency, such as dark skin or not enough sunlight, is unlikely to be corrected in the future.  We have observed that it takes at least 6 months taking regular vitamin D for symptoms to resolve and the level of vitamin D to return to normal.  It should be noted that if you have severe deficiency the doctor may recommend that you take a higher dose of vitamin D for a limited time, often equivalent to 25ug for the first 3 months.  Please discuss this with your own doctor.  We recommend that patients buy vitamin D tablets as we are unable to prescribe vitamin D without calcium on the NHS and calcium prescriptions have been associated with increased kidney stones and it is for this reason that we recommend that our patients buy vitamin D.

Maintenance therapy after deficiency has been treated

The dose needed for maintenance maybe lower than that stated.  We advise patients to buy 10ug and take 2 a day.   When the body's stores of vitamin D have been replenished. maintenance treatment is often needed long-term, to prevent further deficiency in the future. This is because it is unlikely that any risk factor for vitamin D deficiency in the first place, will have completely resolved. The dose needed for maintenance may be lower than that needed to treat the deficiency.

Cautions when taking vitamin D supplements

Care is needed with vitamin D supplements in certain situations:

 1. If you are taking certain other medicines that can interact such as  Digoxin (for an irregular         heartbeat – atrial fibrillation),  Thiazide or diuretics (water tablets).                                                   

2. If you have medical conditions such as kidney stones, some types of                                                     kidney disease, liver disease or hormonal disease.

3. Vitamin D should not be taken by people who have high calcium levels.

4. You may need more than the usual dose if taking certain medicines such as Carbamezapine, Phenytoin. HRT or barbiturates. Multivitamins are not suitable for long-term high-dose treatment because the vitamin A which can be harmful in large amounts.

Are there any side-effects from vitamin D supplements?

It is very unusual to get side effects from vitamin D if taken in the prescribed dose. However, very high doses can raise calcium levels in the blood. This would cause symptoms such as thirst, passing a lot of urine, nausea or vomiting.

Prognosis (outlook) in vitamin D deficiency?

The outlook for vitamin D deficiency is usually excellent. Both the vitamin levels and the symptoms generally respond well to treatment. However, it can take time (months) for symptoms to resolve and for bones to recover.  Generally after 6 months of using Vitamin D tablets the patient feels a lot better and symptoms have improved.  This does not mean you need to stop taking the medication.  Vitamin D supplementation is for life.

Pigmentation and Discoloration of Oral and Facial Tissues

Pigmentation and Discoloration of Oral and Facial Tissues

Pigmentation is a discoloration of the oral mucosa or gingiva due to the wide variety of lesions and conditions. Oral pigmentation has been associated with a variety of endogenous and exogenous etiologic factors. Also it can be explained as Oral mucosal discolouration, which ranges from brown to black may be due to superficial (extrinsic) or deep (intrinsic in or beneath mucosa) causes.

Types of Oro-maxillofacial Pigmentation

Extrinsic discoloration

Extrinsic discoloration is usually caused by extrinsic pigments. It is rarely of consequence and is usually caused by colored foods, drinks or drugs. Extrinsic discoloration usually affects both mucosae and teeth are discolored. Causes include the following:

• Foods and beverages, such as beetroot, red wine, coffee and tea.

• Confectionery, such as liquorice.

• Drugs, such as chlorhexidine, iron salts, griseofulvin, crack cocaine, minocycline, bismuth subsalicylate, lansoprazole and HRT.

• Tobacco: this may cause extrinsic discolouration, but can also cause intrinsic pigmentary incontinence, with pigment cells increasing and appearing in the lamina propria. This is especially likely in persons who smoke with the lighted end of the cigarette within the mouth (reverse smoking), as practiced mainly in some Asian communities. Tobacco is a risk factor for cancer.

• Betel: this may cause a brownish-red discolouration, mainly on the teeth and in the buccal mucosa, with an irregular epithelial surface that has a tendency to desquamate. It is seen mainly in women from South and Southeast Asia. Betel chewer’s mucosa epithelium is often hyperplastic, and brownish amorphous material from the betel quid may be seen on the epithelial surface and intra- and intercellularly, with ballooning of epithelial cells. Betel chewer’s mucosa is not known to be precancerous, but betel use predisposes to submucous fibrosis and to cancer.

Intrinsic staining

Causes for intrinsic hyperpigmentation are Increased melanin or number of melanocytes, or other materials. Intrinsic discolouration may have more significance than the extrinsic type. Normal intrinsic pigmentation is due to melanin, produced by melanocytes dendritic cells prominent in the basal epithelium.

Localized areas of pigmentation are usually caused by benign conditions:

• Embedded amalgam (amalgam tattoo)

• Embedded graphite (graphite tattoo)

• Other foreign bodies

• Local irritation/inflammation

• Melanotic macule

• Naevi

• Melanoacanthoma.

However, neoplasms, such as Kaposi sarcoma or malignant melanoma, are occasionally responsible. The anterior pituitary gland releases melanocyte stimulating hormone (MSH), which increases melanin production. Melanin pigmentation thus increases under hormonal stimulation, either by MSH, or in pregnancy, or rarely due to the action of adrenocorticotrophic hormone (ACTH), the molecule of which is similar to MSH, or under the influence of other factors (e.g. smoking). Thus in all patients systemic causes should be excluded, such as:

• Drugs; including smoking and the contraceptive pill

• Hypoadrenalism; there is increased ACTH production

• Peutz–Jeghers syndrome

• HIV infection

• Von Recklinghausen’s disease

• Albright syndrome

• Rarely, palatal pigmentation from bronchogenic carcinoma.

Amalgam Tattoo

Betel Stains

Peutz Jeghers Syndrome

List Causes of hyperpigmentation

Localized

• Amalgam, graphite, carbon, dyes, inks or other tattoos

• Ephelis (freckle)

• Epithelioid angiomatosis

• Kaposi’s sarcoma

• Malignant melanoma

• Melanoacanthoma

• Melanotic macule

• Naevus

• Pigmented neuroectodermal tumour

• Verruciform xanthoma

Multiple or generalized

Genetic:

• Racial

• Carney syndrome

• Complex of myxomas, spotty pigmentation and endocrine overactivity

• Laugier–Hunziker syndrome

• Lentiginosis profusa

• Leopard syndrome

• Peutz–Jeghers syndrome

Drugs:

• ACTH

• amiodarone

• antimalarials

• betel

• busulphan

• chlorpromazine

• clofazamine

• contraceptive pill

• ketoconazole

• menthol

• metals (bismuth, mercury, silver, gold, arsenic, copper, chromium, cobalt, manganese)

• methyldopa

• minocycline

• phenothiazines

• smoking

• zidovudine

Endocrine:

• Addison’s disease

• Albright’s syndrome

• Nelson’s syndrome

• pregnancy

Post-inflammatory

Others:

• Gaucher’s disease

• generalized neurofibromatosis

• haemochromatosis

• HIV disease

• incontinentia pigmenti

• thalassaemia

• Whipple’s disease

 

List the Causes of Pigmentation 

Melanin

Melanin, a nonhemoglobin derived brown pigment, is the most common of the endogenous pigments and is produced by melanocytes present in the basal layer of the epithelium. Melancocytes have a round nucleus with a double nucleus membrane and clear cytoplasm lacking desmosomes or attachment plates. Melanin accumulates in the cytoplasm, and the melanosome is transformed into a structureless particle no longer capable of melanogenesis. The number of melanocytes in the mucosa corresponds numerically to that of skin; however,in the mucosa their activity is reduced. Various stimuli can result in an increased production of melanin at the level of mucosa including trauma, hormones, radiation, and medications.Thyrosinase activity is present in premelanosome and melanosomes but absent in melanin granules.

Melanoid

Granules of melanoid pigment are scattered in the stratum lucidum and stratum corneum of the skin. Initially it was assumed melanoid was a degradation product of melanin, but more recently it has been shown that such a relationship is highly improbable. Melanoid imparts a clear yellow shade to the skin.3

Oxyhemoglobin and Reduced Hemoglobin

Oxyhemoglobin and reduced hemoglobin are pigments resulting from hemosiderin deposits.

The skin color is affected by the capillary and venom plexuses shining through the skin.

Carotene

Carotene is distributed in the lipids of the stratum corneum and stratum lucidum and gives a deep yellow color to the skin. It is found in higher concentrations in more women than in men. Pigmented lesions of the oral cavity are of multiple origin. Different classifications are used at this time. Some researchers divide the lesions into two main groups as either endogenous or exogenous lesions. Brocheriou et al.

subdivides pigmented lesions as follows:

• Non tumoral pigmentations

• Non melanin pigmented tumors or tumor like lesions

• Benign melanin pigmented tumors

• Malignant melanomas

In several articles on oral pigmentation, Dummett and others implicate many systemic and local factors as causes of changes in oral pigmentation.

Epidemiology

Oral pigmentation occurs in all races of man.There were no significant differences in oral pigmentation between males and females. The intensity and distribution of racial pigmentation of the oral mucosa is variable, not only between races, but also between different individuals of the same race and within different areas of the same mouth. Physiologic pigmentation is probably genetically determined, but as Dummett suggested , the degree of pigmentation is partially related to mechanical, chemical, and physical stimulation. In darker skinned people oral pigmentation increases, but there is no difference in the number of melanocytes between fair-skinned and dark-skinned individuals. The variation is related to differences in the activity of melanocytes.There is some controversy about the relationship between age and oral pigmentation. Steigmann and Amir et al. stated all kinds of oral pigmentation appear in young children. Prinz, on the other hand, claimed physiologic pigmentation did not appear in children and was clinically visible only after puberty.

Clinical Characteristics

The gingivae are the most frequently pigmented intraoral tissues. Microscopically, melanoblasts are normally present in the basal layers of the lamina propria.The most common location was the attached gingiva (27.5%) followed in decreasing order by the papillary gingiva, the marginal gingiva, and the alveolar mucosa.The total number of melanophores in the attached gingival was approximately 16 times greater than in the free gingival. The prevalence of gingival pigmentation was higher on the labial part of the gingiva than on the buccal and palatal/lingual parts of the arches.The shade of pigment was

classified as very dark brown to black, brown, light brown-yellow.3 Melanin pigmentation of the

oral tissues usually does not present a medical problem, but patients complain of black gums.

Classification and Differential Diagnosis

Oral pigmentation has been associated with a variety of lesions and conditions. Differential diagnosis of oral mucous membrane pigmentations are made according to the following situations:

A. Localized Pigmentations: Amalgam tatoo, graphite or other tattoos, nevus, melanotic macules, melanoacanthoma, malignant melanoma, Kaposi’s sarcoma, epithelioid oligomatosis, verruciform xanthoma

B. Multiple or Generalized Pigmentations

1. Genetics: Idiopathic melanin pigmentation (racial or physiologic pigmentation), Peutz-Jegher’s syndrome, Laugier-Hunziker syndrome, complex of myxozomas, spotty pigmentation, endocrine overactivity, Carney syndrome, Leopard syndrome, and lentiginosis profuse

2. Drugs: Smoking, betel, anti-malarials, antimicrobials, minocycline, amiodarone, clorpromazine, ACTH, zidovudine, ketoconazole, methyldopa, busulphan, menthol, contraceptive pills, and heavy metals exposure (gold, bismuth, mercury, silver, lead, copper)

3. Endocrine: Addison’s disease, Albright’s syndrome, Acanthosis nigricans, pregnancy, hyperthyroidism

4. Postinflammatory: Periodontal disease, postsurgical gingival repigmentation

5. Others: Haemochromatosis, generalized neurofibromatosis, incontinenti pigmenti, Whipple’s disease, Wilson’s disease, Gaucher’s disease, HIV disease, thalassemia, pigmented gingival cyst, and nutritional deficiencies

Systemic and Local Causes of Pigmentation

Many systemic and local factors are caused by changes in oral pigmentation. Some of the important factors are discussed below.

Amalgam Tattoo

The pigmentation of the oral mucous membrane by tooth restoration material (amalgam) is a

common finding in dental practice. Amalgam pigmentation is generally called amalgam tattoo.The lesion represents embedded amalgam particles and usually manifests itself as an isolated bluish or black macule in various areas of the mucosa. The color is usually described as black, blue, grey, or a combination of these. Almost half were located on the gingiva and alveolar mucosa, the mandibular region being affected more than the maxillary region. Almost half of the lesions were asymtomatic and were discovered during routine dental examination. The amalgam granules and fragments were found mainly in the lamina propria but were sometimes seen in the submucosa.

Pigmented Nevi

Pigmented nevi of the oral cavity are uncommon. The pigmented nevi are classified as intramucosal, junctional, compound, or blue according to their histological features. Nevi are seen particularly on the vermillion border of the lips and the gingivae. They are usually grey, brown, or bluish macules and are typically asymptomatic. Melanocytes are pigment producing cells characterized by the ability to syntesize via the enzyme dihydroxyphenylalanine (DOPA). A group of melanocytes (generally four or more) are in contact with the basal layer of the epithelium.

Oral Melanotic Macules

Oral melanotic macules are relatively rare oral mucosal lesions, analogous to skin freckles, due to the focal increase of melanin production.These melanotic macules have been variously termed ephelis, melonosis, lentigo, solitary labial lentigo, labial melanotic macule, and oral melanotic macule.The vermillion border of the lower lip is most commonly involved.The buccal mucosa, palate, and gingiva are less commonly affected. The color is usually described as grey, brown, blue, black, or a combination of these.Histologically, ephelis shows increased melanin pigmentation in the basal cell layer without an increase in the number of melanocytes; otherwise, the epidermis is normal.

Melanoma

Melanoma is a cancerous condition of the melanocyte. Special corpusles in this cell, known as melanosomes, contain the necessary enzyme (tyrosine) to transform amino acids into melanin. Melanocytes are found among the basal cells of the epidermis. Histopathogically, the mucosal epithelium is abnormal with large atypical melanocytes and excessive melanin. Malignant melanoma of the oral mucosa affects both sexes equally usually after 40 years of age. The great majority of the lesions (about 70-80%) occur on the palate, upper gingival, and alveolar mucosa.Initially there usually is a solitary small asymtomatic brown or black macule.

Physiologic Pigmentation

Physiologic pigmentation of the oral mucosa is clinically manifested as multifocal or diffuse melanin pigmentation with variable prevalence in different ethnic groups.2 Melanin is normally found in the skin of all people. In dark skinned persons the gingiva may contain melanin pigment to a greater extent than the adjacent alveolar mucosa. The melanin pigment is synthesized in specialized cells, the melanocytes, located in the basal layer of the epithelium. The melanin is produced as granules. The melanosomes are stored within the cytoplasm of the melanocytes, as well as in the cytoplasm of adjacent keratinocytes. Melanocytes are embryologically derived from neural crest cells that eventually migrate into the epithelium. If pigmented gingiva is surgically resected, it will often heal with little or no pigmentation; therefore, surgical procedures should be designed so as to preserve the pigmented tissues.

Peutz-Jeghers Syndrome

Peutz-Jeghers syndrome (intestinal polyposis) is a genetic disorder characterized by mucocutaneous pigmentation and hamartomas of the intestine.It manifests itself as frecklelike macules about the hands, perioral skin, and intraorally to include the gingiva, buccal, and labial mucosa. Pigmented spots are 1 to l0 mm in diameter. Pigmented spots are particularly found on the lower lip and buccal mucosa but rarely on the upper lip, tongue, palate, and gingiva.

Smoker’s Melanosis

Smoker’s melanosis is a benign focal pigmentation of the oral mucosa. It tends to increase significantly with tobacco consumption. Tobacco smokers have significantly more oral surfaces pigmented than non-tobacco users.Clinically, the lesion usually presents as multiple brown pigmented macules less than 1 cm in diameter, localized mainly at the attached labial anterior gingival and the interdental papillae of the mandible. Smoker’s melonosis is more common in females usually after the third decade of life.

Antimalaria Drug Use

Several antimalarial drugs are known to be capable of inducing intraoral melanin pigmentation. These drugs include: quinacrine, chloroquine, and hydroxychloroquine Longterm use may cause pigmentation of the oral mucosa. The pigmentation of the oral mucosa is described as slate-grey in color, bearing some resemblance to pigmentation caused by silver arsplenamine.

Minocycline Use

Minocycline is a synthetic tetracycline that is commonly used in the treatment of acne vulgaris.Although tetracycline causes pigmentation of bones and teeth, minocycline alone is also responsible for soft tissue pigmentation.It is usually seen as brown melanin deposits on the hard palate, gingiva, mucous membranes, and the tongue.

Heavy Metals

Heavy metals absorbed systemically from therapeutic use or occupational environments may discolor the gingiva and other areas of the oral mucosa. Bismuth, arsenic, and mercury produce a black line in the gingiva which follows the contour of the margin. Lead results in a bluish red or deep blue linear pigmentation of the gingival margin (Burtonian line). Exposure to silver causes a violet marginal line, often accompanied by a diffuse bluish-grey discoloration throughout the oral mucosa.

Addison’s Disease

Addison’s disease or primary adrenocortical hypofunction is due to adrenocortical damage

and hypofunction.Bronzing of the skin and increased pigmentation of the lips, gingivae, buccal mucosa, and tongue may be seen. Oral pigmentation may be the first sign of the disease.A biopsy of the oral lesions shows acanthosis with silver-positive granules in the cells of the stratum germinativum. Melanin is seen in the basal layer.

Periodontal Diseases

Periodontal diseases often produce discolorations of the oral mucosa. The pigmentation is worsened by gingivitis, which increases vascular permeability and allows the heavy metals access to the soft tissues.51 Melanin re-pigmentation is related to after surgical inury.

Hemachromatosis

Hemachromatosis (bronze diabetes) is a chronic disease characterized by the deposition of excess iron (ferritin and hemosiderin) in the body tissues, resulting in fibrosis and functional insufficiency of the involved organs. Hyperpig mentation may appear both in skin and mucous membranes (oral and conjunctiva). Gingival or mucosal pigmentation is reported to occur in 15 to 25% of patients with hemachromatosis. The oral mucosa shows diffuse homogeneous pigmentation of gray-brown or deep brown in about 20% of the cases. The buccal mucosa and the attached gingiva are the most frequently involved sites.

HIV Infection

In patients infected with human immunodeficiency virus (HIV), progessive hyperpigmentation of the skin, oral mucosa, fingernails, and toenails have been reported being related to primary adrenocortical deficiency and to zidovudine (azidothymidine) therapy in some cases.Clinically, oral pigmentation appears as irregular macules with brown or dark brown color. The tongue, buccal mucosa, and palate are the most commonly affected sites.