Saturday, May 11, 2013

Diabetes education booklet

Introduction to diabetes
Approximately 1.4 million people in the UK have diabetes and it is suggested by Diabetes UK that there could be another one million people with diabetes and are unaware they have it. The majority of people with diabetes (85% - 90% will have Type 2 diabetes). The remainder will have Type 1 diabetes.
Diabetes Mellitus is a condition in which the amount of sugar in the blood is too high. When we eat a meal the starchy and sugary carbohydrates are changed into sugar (glucose ) during dijestion and this sugar then  passes into the bloodstream. When the pancreas senses that there is a rising level of glucose in the blood it secretes a hormone called insulin. Insulin changes glucose into energy which provides fuel for the body. Insulin is vital for life because without it, the glucose could not be changed into energy and the body could not function without energy. It is often said that insulin acts like a key – unlocking the cell to allow the energy in. Obviously, like a car, we only need a certain amount of energy to provide for the requirements of the body. If we eat more than we need this will be stored as fat.

Signs and symptoms of diabetes
·         Excessive thirst
·         Frequency in  passing of urine
·         Blurred vision
·         Loss of weight
·         Tiredness
·         Mood changes
·         Frequent infections e. boils, thrush etc


Types of diabetes

There are two main types of diabetes:
·         Type 1 ( used to be called insulin dependent ) affecting children and young adults mostly
·         Type 2 diabetes ( used to be called non insulin dependent ) is commoner in the over 40 year olds although children as young as sixteen and obese are alsodeveloping Type2 diabetes

 Main Aim of treatment
The main aim of treatment of both types of diabetes is to normalise blood glucose levels to protect against long term damage to the eyes, kidneys, nerves,
heart and all the blood vessels. Some experts call diabetes “a blood vessel disease”  because preventing narrowing of the blood vessels is key to preventing complications.


Type 1 diabetes

The exact cause of Type 1 diabetes is unknown but thought to be due to a viral infection or environmental factors. In type 1 diabetes there is total destruction of the cells in the pancreas  ( beta cells ) that produce the insulin. The onset of type1 diabetes is acute, because as stated earlier insulin changes glucose into energy but in the absence of insulin, glucose builds up in the blood and is not turned into energy. In an effort to overcome the lack of fuel for the normal functioning of the body, fats and proteins are broken down instead. This is why
patients are often underweight at diagnosis.
Once treatment with insulin is started the patient will begin to feel better quickly and will regain the lost weight.

Treatment for type1 diabetes
People with Type 1 diabetes will need injections of insulin for the rest of their lives. Insulin is destroyed by the gastric juices so cannot be taken in tablet form.
People with Type1 diabetes will need a minimum of two injections daily and often more. They will also need to eat a healthy diet and take regular exercise and do regular self blood glucose testing
If you have been diagnosed with Type 1 diabetes please ask your health professional for the special  section on “ Insulin Ttreatment” which will give you much more specific and detailed information.


Type 2 diabetes

Type 2 diabetes occurs when the pancreas secretes less insulin than normal or when the insulin secreted fails to work properly (called insulin resistance). People who are overweight are five times more likely to develop Type 2 diabetes and four out of five people with Type 2 diabetes are overweight. Excess weight increases your body’s own glucose production and thus your body’s need for insulin too. At the same time, this extra insulin increases fatty acids stores and further increases insulin resistance. It becomes a vicious circle.
Type 2 diabetes is particularly associated with central excess weight ( apple shaped rather than pear shaped). Health risks increase when waist circumference is greater than 37inches (94cms) in men and 31.5 inches (80cms ) in women. Reducing calorie intake if you are overweight will help your body use insulin better by reducing insulin resistance.
You will find a whole section of this book devoted to healthy eating, weight control and exercise.

Type 2diabetes has a gradual onset. You may not feel any symptoms beyond a little tiredness which is often mistakenly attributed to age and working hard. As Type2 diabetes progresses  you may become aware of some of the signs already mentioned or you may be diagnosed  whilst being investigated for something else. It is suggested by experts that most people have had Type2 diabetes for at least five years before diagnosis.

The following people are at an increased risk of developing Type2 diabetes:
  • Family history of diabetes
  • Asian or Afro-Caribean origin
  • Women who have had gestational diabetes
  • Obese people
  • People who take little exercise
  • Older age
  • People on certain medications eg steroids, and some anti psychotic medications

Treatment for Type2 diabetes

People with Type2 diabetes will be encouraged to eat a healthy balanced  diet and take regular exercise. They will be treated with diet only for the first three months after diagnosis (unless their blood glucose is very high and they are losing weight). If diet and exercise alone does not control your blood glucose levels you may also need to take tablets.

Diabetes and Driving in UK

Having diabetes does not mean that you cannot drive as long as you doctor says you are safe to do so – this is usually when your diabetes becomes stable and controlled. You will however have to plan in advance before getting behind the wheel of your car if you are on certain tablets for your diabetes and/or taking insulin.

You must by law inform the Driver and Vehicle Licensing Agency (DVLA) if
  • Your diabetes is treated with tablets or insulin
  • If your treatment changes from tablets to insulin or if insulin is added to the tablets
  • If there are changes in your health or condition that may affect your ability to drive safely
  • If you are applying for a licence for the first time, you must answer YES to the question about diabetes.

People Treated with Insulin
After you have written to the DVLA informing them of your insulin treatment, you will be sent a form (called “Diabetic 1”), asking for more information and for the name and address of your GP/ Hospital Doctor. You will be asked to sign a consent form allowing the DVLA to contact the doctor directly for more specific information on your diabetes control, eyesight and general fitness to drive.
This does not mean that you will be refused a licence – it just ensures safety for you and other drivers. Please answer all questions fully and honestly.


People Treated with Tablets

After you have informed the DVLA that you have diabetes, they will send you a letter explaining your responsibility to re-notify them if you start having insulin or have “hypos” (low blood sugar), or if you develop any of the complications of diabetes which could affect your ability to drive.
They will not normally ask you any other questions at this stage and you will normally expect to keep your “till to” licence.

Diet alone Treated patients

No restrictions on driving and do not need to inform DVLA.

Restricted Licences
Insulin treated – a driving licence will be issued to you for one, two or three years if you are treated with insulin. Just before expiry date, you will receive a reminder to renew your licence and you will be asked to return your current licence. You will be sent another “Diabetic1” form to confirm your medical condition. Renewals of restricted licences are free.
Tablets or diet treated – usually issued with a “till to” licence. When you reach 70 years of age, you will be expected (like everyone else in UK) to renew it every one to three years. There is a charge for this renewal.

Provisional licences – applies to insulin treated only – need to be renewed every one, two or three years.

When renewing licences, it is always sensible to keep a copy of the old licence or to make a note of the driver number, before sending to the DVLA. The process takes between six – eight weeks unless there are complications.

If you drive a motorcycle the rules for informing the DVLA are the same as for a car.
Eyesight Problems
Obviously it is important to have good distance vision and good field of vision (what you can see side to side when looking straight ahead). There are various tests that an ophthalmologist can do to carry out to test these factors. Your licence may be revoked if you fail a field of vision test, but you can appeal against it. There are different types of field of vision tests, some people do better on one type versus another. The DVLA will accept the results of any approved type of test.

Large Goods Vehicles (LGV) and Passenger Carrying Vehicles (PCV)
In 1991 the titles of HGV (heavy goods vehicle) changed to LGV
                    And PSV (public services vehicles) changed to PCV.
People treated with diet alone or diet and tablets are normally allowed to hold LGV and PCV licences, provided they are otherwise in good health.

People treated on insulin are not allowed to hold these licences. If you currently hold such a licence and start using insulin you must inform the DVLA and stop driving the vehicle immediately.
In 1996, the regulation on larger vehicles was extended to include medium sized vehicles. Anyone passing their driving test after 31st December 1996 will only be given a licence to drive vehicles up to 3.5 tonnes.

Vehicles weighing 3.5 tonnes – 7.5 tonnes (Category CI ) and mini buses (DI) are now treated as Group 2 vehicles – normally there is a complete ban on insulin users obtaining a group 2  licence. However some CI licence holders can now apply for a medical assessment and can regain ability to drive these vehicles whilst on insulin. Please write to the DVLA for more information.

Taxis
The law does not bar insulin users from driving taxis, provided they are less than nine seats. As local councils issue licences the policy may vary in different parts of the UK. Some taxi authorities issue blanket restrictions. Please contact Diabetes UK and DVLC for more information.

Diabetes in Pregnancy (Gestational Diabetes)
If you need to commence insulin in pregnancy, you should notify DVLA immediately.
You will normally be allowed to continue driving but are recommended to stop if your control becomes unstable or if you do not have good warning signs of hypoglycaemia. You should re notify the DVLA six weeks after delivery if you are still on insulin, as your licence will need to be reassessed.
If you have problems relating to your driving licence, please discuss it with your diabetes team, who will be able to advise you. DVLA wish to issue licences, not to take them away – you can help by giving as much information as possible.

DO NOT DRIVE IF
·         You have difficulty recognising early signs of hypoglycaemia  (Section   )
·         You have started on insulin and your diabetes is not yet controlled.
·         You have problems with eyesight not corrected by glasses
·         You have numbness or weakness in your feet caused by nerve damage or circulation (neuropathy or ischaemia)
·         You have been drinking alcohol.

Precautions before Driving
  • Long journeys need careful planning, allowing for regular stops if you are on specific tablets for diabetes and insulin.
Normally it is wise to have something to eat every two to three and half hours if you are on insulin and not to miss meals and not to delay meals if you are on tablets and insulin.
  •  Test your blood sugar before driving and regularly during a long drive or if at work before you drive home at the end of the day or shift.
  • ·Always carry quick acting glucose and slow release carbohydrate in the car at all times if you are on insulin or specific diabetes tablets.
  • Always carry identification on your person and in the car stating your name, how your diabetes is treated and the name of your GP.

At the first sign of Hypoglycaemia
·         Stop driving as soon as it is safe to do so
·         Remove ignition key and move into passenger seat.
·         Immediately take glucose tablets or sugary drink (both may be required)
·         Follow this with slow release carbohydrate i.e sandwich, crisps, biscuits etc.
·         Wait for at least 15 – 20 minutes until you feel better, recheck blood if possible, if you do not feel better, take more glucose and biscuits and wait a further 15 minutes.
·       If you continue to feel unwell – call for help and do not drive – if considering using motorway emergency assistance, please remember you may be unsteady on your feet, so take extra glucose before walking.

Car Insurance
 The main potential danger of diabetes and driving is the possibility of having a hypoglycaemic episode which could impair your judgement and lead to an accident.
Since the Disability Discrimination Act came into effect at the end of 1996, insurers can only refuse cover if they have evidence of increased risk.
It is virtually important to inform your motor insurance that you have diabetes.
Your motor insurance may become invalid if
·         You fail to update them on changes to your treatment or physical condition
·         You fail to notify the DVLA as mentioned previously
·         You fail to comply with DVLA restrictions or recommendations
Diabetes UK Services   has an exclusive service that will search through a panel of insurers for the best quote,  - freephone 0800 731 7431.

Life Assurance / Insurance
Some people experience difficulty getting life cover. It is important that you declare your diabetes when applying for a new policy. Any life policy you hold at the time of diagnosis is unaffected.
Any difficulties ring Diabetes UK Careline 0845  120 2960
Or write to Diabetes UK Careline, 10, Parkway, London, NW1 7AA (operates a translation service also)

Travel Insurance
Many travel insurance policies exclude pre-existing medical conditions such as diabetes, you must check carefully if your policy includes or excludes diabetes.
Some insurance companies charge an extra £10 - £15 to include diabetes. It is worth having a letter to this effect from the insurers
Diabetes UK are continually expanding the service they offer. Please see relevant telephone lists at the back of this booklet.

Diabetes and Employment
An employer cannot by law refuse to employ you or dismiss you purely because you have diabetes, according to the Disability Discrimination Act (DDA1995).
Although most people with diabetes do not consider themselves to have a disability, diabetes is covered by the Act.
Certain professions are exempt from the DDA and can refuse to employ someone with diabetes, especially if they are treated with insulin, these include
·         Air line crew
·         Armed services
·         Off shore workers
·         Train drivers
·         Any work requiring LGV and PCV
·         Police force
However, if diabetes is diagnosed whilst in this employment, it may be possible to continue with some negotiable changes in your duties. 

Oral Medicine OSCE Questions-Guess the condition

This patient is a 28 year old male presented to the clinic with a 1 month history of chronic ulceration. n. The oral ulceration caused the patient considerable discomfort and significantly affected his normal oral function. ulcers appeared spontaneously and there was no improvement with the medication he had.Initially lesions appear as blisters and they coalesce to make a ulcer. His past medical history was not significant. Intra oral examination revealed that bilateral buccal mucosa, Gingiva and palate is affected with similar type of ulcers on the lips. Dermatologist confirmed that the patient had cutaneous lesions.

Guess the condition ???

(Please type your answers on the comment box)


Friday, May 10, 2013

Pathology of Oral Cavity Short notes



Manifestations of diseases of the oral cavity

Pain- the oral cavity- richly supplied with sensory nerve endings- pain is a feature  of all diseases, including disorders of the teeth
Changes of the oral mucosa- such as ulcerations, vesicular lesions (blisters), changes in colour

Ulcers- occur in many diseases, including infections, allergy, trauma, and neoplasns
Blisters- infections, such as herpes virur, and immunologic diseases
Leukoplakia- white plaques on the mucosa- in hyperkeratosis, in dysplasia
Melanin pigmentation- Peutz-Jeghers syndrome-is rare congenital syndrome with autosomal dominance, characterized by melanotic pigmentation of mucosal and skin surfaces, and increased risk of carcinoma of pancreas, breast, lung and ovary, in addition patients have multiple polyps in small intestine and colon
Addison disease -uncommon condition characterized by melanin pigmentation of skin and mucosa following destruction of the adrenal cortex, this results in increased stimulation of pituitary gland, high level of ACTH and MSH
Mass lesions- solid or cystic

Non-neoplastic disorders of the oral mucosa
  • Developmental anomalies
  • White lesions and  patches
  • Infections
  • Pseudotumors


Developmental anomalies

Oral mucosa is subject to the same range of developmental anomalies such as skin, and may be involved in head and neck syndromes, but also there are anomalies confined to the oral mucosa itself

1. Fordyce spots- heterotopic development of sebaceous glands in oral mucosa- produce yellow spots and nodules

2. Peutz-Jeghers syndrome- (periorifacial lentiginosis)- autosomal dominant condition with nearly complete penetrance, it is composed of melanocytic macular pigmentation of the lips, oral mucosa, skin together with intestinal polyposis, most numerous hamartomatous polyps in small intestine, the polyps have a low malignant potential, those in colon with higher risk
-the patients are in higher risk of malignancies at other sites, including ovary, uterus and breast
-the facial pigmentation is around lips, eyes and nose and may disappear in adulthood
-mucosal pigmentation tends to persist to adulthood

3. Congenital epulis- present at birth as mass attached to the gingiva, histologically composed of large granular cells with eosinophilic cytoplasm, covered by stratified hyperplastic squamous epithelium- completely benign

White  patches.
White sponge naevus- is rare autosomal dominant inherited condition, may be  congenital or develop later in life
mainly affects buccal mucosa, may involve lips and other oral mucosa
family  history can be detected in all cases
histologically: there is acanthosis, parakeratosis, and edema with hydropic degeneration of the cells in the stratum spinosum, epithelium is not dysplastic, there is no inflammation, no relation to tumor

Frictional keratosis- is a common cause of intraoral white  patches and may be due to sharp  edges of teeth or to cheek and lip sucking, it is a response to low grade irritation

microscopy may show acanthosis or epithelial atrophy, thick layer of orthokeratosis and prominent granular cell layer, or less commonly hyperparakeratosis with absent granular cell layer
there is no significant dysplasia, but sometimes inflammation of the underlying corium, no relation to tumor development
clinically- the lesions tend to form diffuse keratotic plaques

smoking related keratosis- smoking  can result in intraoral plaque formation
histologically-atrophic or hyperkeratotic epithelium with patchy inflammation and melanin pigment in the underlying corium- pigmentary incontinence-release of melanin from demaged cells
there is no significant dysplasia
may be seen in reverse smokers, who hold the burning end of cigarette inside the mouth, this one may be associated with dysplasia

acute oral candidosis-oral infections with candida albicans are common, it forms creamy white plaques which can be rubbed off to leave a dry, red mucosa
histologically-loose parakeratotic plaques infiltrated by leukocytes (intraepithelial microabscesses) with hyphae- difficult to be seen in HE stained sections but are  readily visualised by  staining with PAS or silver impregnation methods, such as Grocott
wide variety of factors predispose to infection, such as depressed cellular immunity, and inhibition of normal oral flora by broad spectrum antibiotics

chronic hyperplastic candidosis (candidal leukoplakia)-Candida albicans can be present in persistent, adherent  white plaques- solitary or multiple
microscopy- shows a parakeratotic plaque infiltrated by leukocytes, acanthosis and inflammatory infiltrate in the corium, epithelium has elongated rete ridges with thinning of the suprapapillary  epithelium giving a resemblance to cutaneous psoriasis, candidal hyphae can be visualized within parakeratotic layer

hairy leukoplakia- patients infected with HIV frequently develop painless, white plaques on the lateral border of the tongue and occassionally elsewhere in the  mouth

microscopy-shows irregular parakeratosis with or without candidal  hyphae, vacuolated cell with dark  pyknotic nuclei (koilocytes) in the stratum spinosum, no inflammatory infiltrate in the corium, Epstein-Barr capsid antigen can be detected in the epithelial cell nuclei
similar lesions have been reported occasionally in patients receiving immunosupressant drugs following organ transplantations

geographic tongue- relatively  common idiopathic condition typically characterized by areas with loss of papillae, mild chronic inflammation in corium, leukocytic microabscesses in the epidermis

Infections- viral, bacterial and fungal
infections of the oral mucosa are comparatively infrequent given the number of microorganisms present in the mouth
Viral:

1) herpes simplex stomatitis- caused by HSV type 1- common viral infection- usually is subclinical
in only few per cent of infected indiviuals, there are more severe symptoms presenting as widespread gingivostomatitis, characterized by multiple vesicles and ulcers- in children and young adults- systemic symptoms- like fever are present
locally severe, painful, but self-limited disease- healing occurs within two weeks, recurrent infections may be associated with abnormalities of cell-mediated immunity
HS virus passes up the nerve trunks and infects the ganglia in acute phase,  it remains in latent form for long time there

Herpes labialis-in some patients- attacks of reactivation of the infection as painful localized vesicular and ulceral lesion -reactivation is always precipitated by exposure to sunlight, fever, common cold, etc.

2) herpangina -is uncommon infection of the oral mucosa by coxsackie virus A, occurs as vesicular lesion on the palate

3) aphtous stomatitis- common lesion characterized by recurrent attacks of painful shallow ulcers on the oral mucosa- nonspecific acute infiltrate
cause is unknown- no infectious agent has been identified- self-limited lesion

4) viral warts- viral warts of the oral mucosa present as a lesion similar to condyloma accuminatum

histologically: features suggestive of viral etiology such as koilocytosis, numerous mitoses, viral inclusions can be present- detection of HPV DNA sequences  within the tissue using in situ hydridization technique assists in diagnosis- HPV type 6, 11 and 16 will be present (human papilloma virus)

Bacterial:

1.) Acute ulcerative gingivitis:
painful condition with ulceration of the interdental papillae between teeth, the ulcers have irregular margins and are covered with fibrinous exudate  -etiology is unclear, and is partly relate to poor oral hygiene -smears from ulcers show mixed population of spirochetes, and fusiform bacteria

2.) Actinomycosis- infection of oral mucosa by actinomyces presents as swelling of the mucosa, the organisms are normally present in the mouth- infection is opportunistic

3.) Tuberculosis- infection of oral mucosa by tbc bacili is now uncommon, presents with tuberculosis ulcers that are secondary to pulmonary tuberculosis

4.) Syphilis- syphilitic infection of the oral mucosa is rare in this country, the chancre of the primary infect may occur on the lips or inside the mouth, mucous patches and ulcers may develop in secondary stage, and tertiary syphilis may present with gumma in the tongue or palate

Fungal:                

1) candidosis -is caused by Candida albicans, which is present as normal commensal of the mouths of about one-half of the population
clinical infection of the oral mucosa is an example of opportunistic infection- occurs for example in patients with increased susceptibility (with immunosupression, in AIDS, in newborns, in patients receiving anti-cancer therapy or long-lasting antibiotic therapy, patients with diabetes mellitus)
morphology: edema of the epithelium, ulcerations, Candida produces inflammation, white patches- the budding yeasts and pseudohyphae of Candida can be identified in smears and biopsy specimens from the lesions

Pseudotumors  and hyperplastic lesions of the oral mucosa

Epulis -pseudotumors of gingiva -these are reactive lesions of gingiva, grossly- polypoid masses, most common types are

Granulomatous epulis- pyogenic granuloma -reactive inflammatory proliferation of nonspecific granulation tissue
grossly: small, bright red nodule with ulceration of the mucosal surface
it occurs quite commonly in pregnancy-and it resolves spontaneously

Giant cell epulis -distinctive lesion of gingiva composed of multinucleated giant cells and spindle mononuclear cells, giant cell epulides tend to be highly vascularized, there can be considerable amounts of hemosiderin, osseous metaplasia is rather common
not true neoplasm-most likely a reactive lesion, however, the lesion tends to recur after excision

Fibromatous epulis -composed of fibroblasts and myofibroblasts, the lesions show variable degree of cellularity and collagen, dystrophic calcification may occur, osseous metaplasia is common-osteofibromatous epulis

Congenital epulis- usually seen in newborn as a polypoid lesion in the anterior maxilla, often protrude from the mouth as a reddish swelling, histologically - the lesion is composed of large eosinophilic cells with granular cytoplasm- the lesion is entirely benign

Fibrous hyperplasia –common tumor-like swelling of oral mucosa, these lesions are considered to be a response to low grade irritation
polypoid swellings may be sessile and pedunculated
microsopically consist of collagen bundles and moderately cellular fibrous tissue

Papillary hyperplasia –typically seen in hard palate, belong to spectrum of denture-related , induced stomatitits

Generalized gingival fibrous hyperplasia –familiar or drug induced

Hereditary gingival fibromatosis- rare condition with AD trait, may be associated with hypertrichosis, neurological problems, such as epilepsy

Drug-induced gingival hypertrophy- seen in about half of patients treated with anti-epileptic drug phenytoin for long period, other drug may roduce similar- cyclosporin

Orofacial granulomatosis – characterized by chronic granulomatous inflammation of oral mucosa, the cause is unknown, dg after exclusion of Crohns disease, tbc and sarcoidosis
Melkersson-Rosenthal disease-cheilitis granulomatosa,fissured tongue, facial nerve palsy


 Precancerous conditions and tumors of the oral mucosa
The most important neoplasm of the mouth is squamous cell carcinoma- despite the accessibility of the mouth to visual inspection, most oral cancers are detected late and their prognosis is comparable to that of squamous cell carcinoma of the esophagus
other malignancies and benign tumor are rare, except of squamous cell papilloma, and salivary gland-derived tumors of the oral mucosa       

Benign tumors of oral mucosa
Benign tumors in the oral cavity may arise - from squamous epithelium, from  mesenchymal tissue, from the minor salivary glands

Squamous papilloma- are usually small, sessile or pedunculated lesions
tehy are composed of fibrovascular core, extensions of which are covered by acanthotic stratified squamous epithelium- no evidence of dysplasia, but koilocytic metaplasia may be present
majority of papillomas are viral in origin-

koilocytosis is a feature of viral infections -koilocytes- clear cell with polymorphic hyperchromatic nucleus pushed to one side
there is no tendency for malignant change

Fibroma, lipoma, neurofibroma- benign mesenchymal tumors

Granular cell tumor- (myoblastoma)- is  not  uncommon tumor of the skin and mucosal surfaces, they arise particularly in the mouth, where the dorsum of  the tongue is a typical site,

histologically-striking pseudoepitheliomatous hyperplasia of the overlying epithelium with usually incospicuous granular cell tumor in  the corium (simulates squamous cell carcinoma), the tumor consists of large cells with abundant finely granular cytoplasm- these cells were once thought to originate from muscle cells, however despite the fact that they seem to fuse with muscle, they appear to be of Schwann cell origin

Oral  pre-malignancies
There is a wide range of mucosal disorders in which squamous cell carcinoma has been shown to develop more easily

Pre-malignant lesions- which show histologically detactable mucosal changes

Pre-malignant conditions- more widespread or systemic disorders affecting oral mucosa where cancer is statistically more likely to develop- although the site is unpredictable

pre-malignant lesions include: for example leukoplakia, palatal changes associated with smoking, and
pre-malignant conditions- sideropenic atrophy and dysphagia caused by iron deficiency
               
LEUKOPLAKIA- this is a term best defined clinically to denote a white patch or plaque
according to this definition - heterogenous group of lesions among which epithelial dysplasias- have pre-malignant potential
 in most cases leukoplakia represents only simple hyperkeratosis resulting from chronic irritation, in minority of cases- there is dysplasia- persistent leukoplakia should be biopsied

Epithelial dysplasia- lesions characterized by disordered cell  maturation and proliferation associated with increased risk of progression to maligancy

histologically-irregular hyperplasia of cells with basal cell morphology, rete ridges show a drop-shaped configuration, loss of both polarity of cells and normal stratification of the epithelium, nuclear changes, such as increased nuclear-cytoplasmic ratio, hyperchromatism and pleomorpism, mitoses in the upper layers of epithellium, abnormal mitoses, individual cell keratinisation often in deep layers (dyskeratosis or premature keratinisation), and loss of celllular  cohesion
-three degrees of dysplasia can be distinguished- mild, moderate, and severe

Malignant tumors of oral mucosa
1) Oral squamous cell carcinoma -accounts for over 90% of all malignant tumors of oral cavity- more common in older men
it is important to consider the site of involvement -most commonly it arises in the lower lip (40%),  lateral margin of the tongue (20%), floor of mouth (15%)- involvement of the upper lip, palate, gingiva and tonsillar area is less common

etiologic factors include cigarette and pipe smoking, alcohol, the lip is more commonly affected in white-skinned people exposed to prolonged sun light- particularly high male predominance

grossly- the  oral cancer mainly presents as an ulcer, lump, or red or white lesion

histologically- majority of oral cancers are well or moderatelly differentiated  squamous cell carcinomas

well-differentiated carcinoma- is composed of epithelial islands which resemble normal stratified squamous epithelium, except that they are invading the underlying tissues and show aberrant abnormal keratinization, there is often a prominent keratin formation in the infiltrating islands, usually strong host response of lymphocytes in the stroma, the tumor may be frankly deeply invasive

poorly differentiated carcinoma- are associated with poorer prognosis, keratin formation is minimal, malignant cells do not exhibit distinction between basal and suprabasal population, mitoses are more frequent, and host response is usually less conspicuous than in better differentiated carcinomas
poorly differentiated carcinomas are sometimes difficult to be distinguished from other malignancies, such as high grade lymphomas, malignant melanomas and sarcomas- correct diagnosis can be helped by means of immunohistochemistry using antibodies against epithelial markers (cytokeratin), mesenchymal markers (vimentin, desmin, actin), and melanoma markers, etc

patterns of spread- muscle, adipose tissue and other connective tissue tend to be invaded readily by oral cancer, salivary gland tissue and bone provide some resistence to invasion

lymph node spread is a relatively late feature of oral cancer- the pattern follows the main anatomical drainage pathways from the primary site- most commonly involved is submandibular lymph node
prognosis and treatment : depends on the stage of the disease and on the site of primary tumor

compared with favourable prognosis for lip cancer- treated by surgery alone or combination of surgery and radiotherapy- five-year survival is around 70%

intraoral cancer has poor prognosis- 5-year survival lower than 40%

other significant adverse factor is the size of tumor at presentation

lymph node metastases, old age (more than 70), and poor histological differentiation- adverse prognostic factors

2) verrucous carcinoma- is a variant of oral squamous cell carcinoma with predominantly exophytic growth pattern, with minimal invasion,
microscopy- shows acanthosis with low degree of epithelial atypia, the advancing margin of the tumor forms pushing margin rather than the finger-like  invasion of squamous cell carcinoma
it tends to have a rather indolent course with minimal if any capacity for metastases- very good prognosis- treatment - only surgery, radiotherapy should be avoided             


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