Ellis classification (Tooth fractures)

Ellis classification (Tooth fractures)

Ellis Class I Enamel fracture: This level of injury includes crown fractures that extend through the enamel only. These teeth are usually nontender and without visible color change but have rough edges. Ellis Class II Enamel and dentin fracture without pulp exposure: Injuries in this category are fractures that involve the enamel as well as the dentin layer. These teeth are typically tender to the touch and to air exposure. A yellow layer of dentin may be visible on examination. Ellis Class III Crown fracture with pulp exposure: These fractures involve the enamel, dentin, and pulp layers. These teeth are tender (similar to those in the Ellis II category) and have a visible area of pink, red, or even blood at the center of the tooth. Ellis Class IV Traumatized tooth that has become non-vital with or without loss of tooth structure. Ellis Class V Luxation: The effect on the tooth that tends to dislocate the tooth from the alveolus. Teeth loss due to trauma. Ellis Class VI Avulsion: The complete separation of a tooth from its alveolus by traumatic injury. Fracture of root with or without loss of crown structure. Ellis Class VII Displacement of a tooth without the fracture of crown or root. Ellis Class VIII Fracture of the crown en masse and its replacement. Ellis Class IX Fracture of deciduous teeth. ------------------------------------ This Article has been edited By :: World Of Dentistry :: TEAM For any questions and suggestions please don't be hesitate to feedback us. Yours, :: World Of Dentistry :: TEAM

Blue Sclera "Definition and Diseases"

Definition:

Blue sclera is characterized by localized or generalized blue coloration of sclera because of thinness and loss of water content, which allow underlying dark choroid to be seen.

Diseases and Disorders:

1. Associated with high urine excretion:A. Folling syndrome (phenylketonuria)
B. Hypophosphatasia (phosphoethanolaminuria)
C. Lowe syndrome (oculocerebrorenal syndrome; chondroitin-4-sulfate-uria)

2. Associated with skeletal disorders:A. Brachmann-de Lange syndrome
B. Brittle cornea syndrome (blue sclera syndrome)-recessive
C. Crouzon disease (craniofacial dysostosis)
D. Hallermann-Streiff syndrome (dyscephalia mandibulooculofacial syndrome)
E. Marfan syndrome (dystrophia mesodermalis congenita)
F. Marshall-Smith syndrome
G. McCune-Albright syndrome (fibrosus dysplasia)
H. Mucopolysaccharidosis VI (Maroteaux-Lamy syndrome)
I. Osteogenesis imperfecta (van der Hoeve syndrome)
J. Paget syndrome (osteitis deformans)
K. Pierre Robin syndrome (micrognathia-glossoptosis syndrome)
L. Robert syndrome
M. Silver-Russell syndrome
N. Werner syndrome (progeria of adults)

3. Chromosome disorders:A. Trisomy syndrome
B. Turner syndrome

4. Ocular:A. Congenital glaucoma
B. Myopia
C. Repeated surgeries
D. Scleromalacia (perforans)
E. Staphyloma
F. Trauma

5. Miscellaneous:A. Ehlers-Danlos syndrome (fibrodysplasia elastica generalisata)
B. Goltz syndrome (focal dermal hypoplasia syndrome)
C. Incontinentia pigmenti (Bloch-Sulzberger syndrome)
D. Lax ligament syndrome
E. Minocycline-induced
F. Oculodermal melanocytosis (nevus of Ota)
G. Pseudoxanthoma elasticum (Grönblad-Strandberg syndrome)
H. Relapsing polychondritis

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Aguesia (Loss Of Tongue's Taste Buds)

Definition:
It's the complete loss of tongue's taste buds .. so that the patient feels nothing of the taste of food ...

Prognosis:
It's not good enough.

Treatment:
1- Artificial saliva and pilocarpine
2- altering the treatment if the cause is a certain therapy.
3- zinc supplements if there is deficiency.
4- zinc infusion with chemotherapy is the patient is treating from cancer.
5- Alpha lipoic acid.

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Melkersson-Rosenthal Syndrome

- Definition:
Melkersson-Rosenthal syndrome is a rare neurological disorder characterised by recurring facial paralysis or palsy, swelling of the face and lips (usually the upper lip), and the development of folds and furrows in the tongue.

- Does it develop in childhood ... ?
Onset is in childhood or early adolescence.

After recurrent attacks (ranging from days to years in between), swelling may persist and increase, eventually becoming permanent. 

The lip may become hard and cracked with a reddish-brown discoloration. 

The tongue may develop furrows.

- Causes:
The cause of Melkersson-Rosenthal syndrome is unknown, but there may be a familial link although a gene has not yet been identified.

- Treatment:
Treatment is symptomatic and may include medication therapies with anti-inflammatory medication and corticosteroids to reduce swelling.

Occasionally surgery may be recommended for severe cases to relieve pressure on the facial nerves and to reduce swollen tissue, but its effectiveness has not been established.

Facial Rehabilitation is available from specialist centers where physiotherapists and speech and language therapists specialized in treatment for people with facial palsy. 

The treatment is similar to the treatment for Bell’s palsy although the causes of the two conditions are different.

- Prognosis:
Melkersson-Rosenthal syndrome may recur intermittently after it first appears.

The person will therefore experience intermittent facial weakness which can resolve as the nerve recovers.

It can become a long standing problem as with each attack recovery is less satisfactory.

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Gingival Hyperplasia

- Enlargement of gums or gingiva is called gingival hyperplasia in the dental terms.

- This occurs due to abnormal multiplication of gingival tissues due to various factors. 

- When an individual is diseased with gingival hyperplasia then the gums become swollen and enlarged. 

- If you are suffering from gingivitis there will be bleeding in the gums as well as tenderness. 

- The teeth get covered with the gums if the infection is too intense. 

- The patient is examined by a dentist and then the patient is sent for further examination if any further complications are seen.

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Causes:

There are several causes of gingival hyperplasia:

- Inflammatory and granulomatous disorders "like Hand-Schuller-Christian syndrome"

- Auto-immune disorders "like plasma cell gingivitis which is associated with allergic and collagenous nature"

- Neoplastic disorders "like acute leukemia and monocytic leukemia"

- Metabolic and storage disorders "like aspartylglycosaminuria, genetic disorders like Cross syndrome"

- Toxicity of drugs.

- Excess of deposition of drugs given to a patient. It is also called as Drug-Induced Gingival Overgrowth (DIGO).

- Immunosuppressant like Cyclosporin, anticonvulsants like valproate, phenytoin, phenobarbital, primidone and calcium channel blockers like nifedipine, verapamil and amlodipine.

Note: Cyclosporin and phenytoin toxicity are the important toxicities caused in a patient especially in case of dental plaque where these drugs get deposited on the tooth.

Causes of Gingival Enlargement is divided into five groups:
- Inflammatory Enlargement
- Enlargement due to systemic /genetic diseases
- Neoplastic enlargement
- False enlargement
- Drug induced enlargement
- Gingival Hyperplasia differential diagnosis

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Diagnosis:

- Mainly done by differential diagnosis.

- IFN-gamma-stimulated gene expression which is important to determine the presence of gingival hyperplasia in the body.

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Treatment:

The treatment of gingival hyperplasia is based on the type and cause of the gingival hyperplasia.

- Improving oral hygiene is the most important factor which will determine the cure rate of the disease.

- Maintain oral hygiene regularly to prevent any further spread of infection.

- Gingivectomy, a surgical procedure to remove the excess of gingival tissue is carried out to manage the condition.

- The drugs which cause toxicities and affect the gingival tissues can be replaced with alternative drug therapies. For instance, in case of immunosupression, cyclosporine can be replaced by tacrolimus which is has less affect in gingival hyperplasia. Nefedipine can be replaced by isradipine as it does not increase the conditions of gingival hyperplasia.

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Dental preparations before Head and Neck Radiotherapy

- The status of the dentition has a significant effect on post-treatment quality of life among patients with head and neck cancer that will undergo radiation.

- A dentition in poor repair will increase the risk of post-radiation complications, particularly dentoalveolar infections that could lead to osteoradionecrosis.

- All patients who will be treated with RT for oral/head and neck cancer should undergo a comprehensive dental evaluation prior to treatment.

- Carious teeth, teeth with deep restorations or in poor periodontal health, along with partial bony impacted third molars should be extracted prior to RT if in an area that is expected to receive a dose of at least 50 Gy.

- Teeth that are out of the radiation treatment field, but have a hopeless prognosis or is symptomatic should also be extracted.

- Extraction of healthy teeth does not appear to prevent the development of osteoradionecrosis.

- All indicated extractions should be completed prior to RT and primary closure over the extraction sites is preferred if possible.

- An adequate alveoloplasty should be performed to eliminated the possibility of bone edges ulcerating the mucosa as well as to make the mandible/maxilla ready for dentures.

- Ideally, all extractions should be completed approximately two weeks before the commencement of RT to permit proper healing.

- If the extracted teeth are outside of the treatment areas, however, radiation may be started sooner.

- The oral surgeon should attempt to do all the extractions within the portals of radiation at one sitting so as not to delay the cancer treatment.

- Postponing needed extractions of teeth that will be within the treatment area until after radiation is associated with an increased risk of non-healing and osteoradionecrosis.

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Vitamin Deficiency and effects in Oral Cavity

- Certain vitamin deficiencies can have serious effects on your mouth and teeth.
- If your mouth is sore or your gums are bleeding, you might not be able to eat well. This can make any vitamin deficiencies worse.

- Seniors are more likely to have vitamin deficiencies because they may have problems absorbing nutrients from food.
- Younger people can also have conditions that cause difficulties absorbing nutrients.
- The physician can determine whether patient have a vitamin deficiency and how it should be treated.
- While dentist can identify oral abnormalities and determine whether a vitamin deficiency is the cause.

Here are some vitamin deficiencies that might affect your mouth and teeth.

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Vitamin B
Vitamin B deficiencies are one of the most common deficiencies that can affect mouth and teeth.

Signs and Symptoms:
- Burning sensation in the mouth, especially on the tongue (Most common oral effects).
- Difficulty in swallowing. The tongue may feel swollen.
- The tissue of the inner cheeks can be pale and may break apart easily and slough off.
- B-vitamin deficiencies also can lead to anemia (too few red blood cells).
- Severe B12 deficiency can cause neurological problems such as numb or tingling limbs.
- Folic Acid deficiency also can make your mouth feel like it's burning.and numb or tingling limbs.
- Folic acid is crucial to fetal development as well. Not having enough of this vitamin during early pregnancy can increase the risk of having a baby with neural tube defects. These are defects of the brain, spinal cord or both.

Risks:
- Angular Cheilitis:
A painful inflammation and cracking in the corners of the mouth. It usually is related to a fungal infection.
- Recurrent Aphthous Stomatitis:
Also known as recurring canker sores. Anemia, which can occur because of vitamin B deficiency, can increase your risk of these sores.
- Chronic Oral Mucosal Candidiasis:
A fungal infection in the mouth, caused by the Candida albicans fungus that is found naturally in the mouth. It does not normally cause problems. However, poor nutrition or poor absorption of vitamins drop down host immunity and tend to change the oral flora.
- Atrophic Glossitis:
A condition that causes the taste buds to break down, making the tongue look "bald." This condition affects the sense of taste. It can occur with a severe vitamin deficiency.

Sources of Vitamins B:
- Thiamin (B1): Pork, whole and enriched grains, legumes, nuts, dried beans
- Riboflavin (B2): Milk and milk products, eggs, liver, almonds, shellfish
- Niacin (B3): Protein-rich foods, meat, liver, poultry, fish, whole grains, peanuts
- Pyroxidine (Vitamin B6): Meat, poultry, fish, leafy green vegetables, bananas, whole grains, legumes, nuts, fruits
- Cobalamin (B12): Fish, meat, poultry, milk and milk products, eggs, fortified cereals
- Folic acid (also called folate): Leafy green vegetables, orange juice, legumes, broccoli, asparagus, fortified cereals, nuts

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Iron:

Signs and Symptoms:
- Burning sensation in the mouth and tongue
- Fungal infections in the mouth
- Tongue redness and swelling
- Sores and pale tissue in the mouth
- Iron deficiency can be caused by a poor diet or by intestinal problems that reduce iron absorption. It also can result from regular blood loss, such as from heavy menstrual periods or internal bleeding.
- Iron deficiency can cause anemia.

Sources of Iron:
- Lean meat
- Leafy green vegetables
- Beans
- Shellfish
- Whole-grain bread

N.B: People with significant iron deficiency may have to take iron supplements.

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Vitamin C
- Vitamin C is also called ascorbic acid.
- This vitamin is needed to make collagen, the main building block for many tissues.

Signs and Symptoms:
- Gingivitis.
- Fatigue and easy Bruising.

Sources of Vitamin C:
- Citrus fruits
- Dark green vegetables
- Tomatoes
- Strawberries
- Peppers
- Cantaloupe

N.B: Smoking depletes vitamin C in the body, so smokers need extra amounts of this vitamin.

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Vitamin A:
Vitamin A helps skin cells grow and maintain themselves.

Signs and Symptoms:
- Delayed healing in the mouth.

Sources of Vitamin A:
- Fortified milk
- Liver (chicken, beef)
- Leafy green vegetables
- Orange and yellow fruits and vegetables (such as apricots, cantaloupe, pumpkin, sweet potatoes and carrots)

N.B: Vitamin A can be stored in body fat, so high-dose supplements are not recommended.
They can cause side effects such as joint pain, headache, diarrhea, fatigue, vomiting and liver damage.

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Vitamin D
Vitamin D works with calcium to maintain bone quality and strength.

Signs and Symptoms:
- Brittle Bones.
- Increase the risks of jaw fracture.
- Increase the risks of periodontal disease.
- A deficiency early in life could affect the formation of teeth.

N.B:
- Sometimes people with kidney disease also have vitamin D deficiency.
- The body will make its own vitamin D if it is exposed to sunlight for several minutes two or three times a week.

Sources of Vitamin D:
- Fish liver oils and fish
- Fortified milk and milk products
- Egg yolk
- Some cereals

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Vitamin K
- Normally, vitamin K is made by bacteria in your intestines.
- Vitamin K helps to make proteins that allow the blood to clot.

Signs and Symptoms:
- Easy bruising.
- Slow healing
- Excessive bleeding after extracted
- Excessive bleeding after scaling.

Sources of Vitamin K:
- Brussels sprouts
- Green leafy vegetables
- Broccoli
- Eggs
- Beef

N.B: A vitamin K deficiency may be caused by liver disease, long-term antibiotic use or other disease(s).

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Scurvy - Vitamin C Deficiency

- Vitamin C is required for the synthesis of collagen in humans.
- The chemical name for vitamin C is Ascorbic Acid.

Causes:
- Scurvy or subclinical scurvy is caused by the lack of vitamin C. In modern Western societies, scurvy is rarely present in adults, although infants and elderly people are affected.
- All Child and Infant Supplements are provided with Vitamin C to avoid Scurvy.
- absence of feeding by the mother breast is one of the most important causes of Scurvy.

Symptoms:
- Early symptoms are malaise and lethargy.
- After 1–3 months, patients develop shortness of breath and bone pain.
- Myalgias may occur because of reduced carnitine production.
- Other symptoms include skin changes with roughness, easy bruising and petechiae, gum disease, loosening of teeth, poor wound healing, and emotional changes.
- Dry mouth and dry eyes similar to Sjögren's syndrome may occur.
- In the late stages, jaundice, generalized edema, oliguria, neuropathy, fever, convulsions, and eventual death are frequently seen.

Prevention:
- Scurvy can be prevented by a diet that includes certain citrus fruits such as oranges or lemons.

- Other sources rich in vitamin C are fruits such as blackcurrants, guava, kiwifruit,papaya, tomatoes, bell peppers, and strawberries.

- It can also be found in some vegetables, such as carrots, broccoli, potatoes, cabbage, spinach and paprika.

Treatment:

Scurvy can be treated by eating food containing vitamin C (such as oranges, papaya, strawberries, lemon), tablets with vitamin C, etc.

Prognosis:

Untreated scurvy is invariably fatal. However, death from scurvy is rare in modern times.

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Lesions of Oral Cavity "Classifications"

Oral Cavity lesions can be seen in different diseases and conditions.
Lesions of the oral cavity may be associated with disease or sometimes hereditary or even normal.
Some lesions even indicate the pre-cancerous condition.
Oral lesions can be broadly classified into four different types.

1. Vesiculo-Bullous lesions
2. Ulcerative lesions
3. White lesions
4. Red lesions

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:: Vesiculo-Bullous lesions ::

These lesions are in the form of superficial blisters of diameter <5mm (vesicle) and >5mm (bulla) usually filled with a clear fluid.

Classification :-

- Hereditary – Epidermolysis bullous dystrophica
- Viral – Small pox, Measles, Chicken pox, Herpes simplex, Herpes zoster, Herpangina, Hand Foot Mouth disease
- Muco cutaneous – Erythema multiforme, Bechet's syndrome , Reiter syndrome, Steven Johnson syndrome
- Immunological – Pemphigus ( vulgaris, vegetans, foliaceous , erythematous),Benign mucous membrane pemphigoid
- Psychosomatic – Bullous lichen planus
- Allergic – Stomatitis medicamatosa, Stomatitis venennata
- Toxicity – Toxic lesions
- Miscellaneous – Submucous fibrosis, Apthous stomatitis, Thermal and Chemical burns.

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:: Ulcerative lesions ::

These lesions are characterized by loss of surface epithelium and frequently some underlying connective tissue. They often appear elevated or depressed.

Classification :-

- Injury - physical, chemical, thermal,radiation, actinic rays
- Infections -
a) Bacterial: Vincent's angina
b) Viral: Herpes simplex ,Herpes zoster, Herpangina
c) Fungal: Candidiasis
- Nutritional deficiencies - protein , B complex
- Allergic - Stomatitis venenata, S.medicamatosa, Fixed drug allergy, Anesthetic reaction during dental extraction.
- Mucocutaneous - Erythema multiforme, Steven-Johnson syndrome, Reiter syndrome, Bechet's disease, Epidermolysis bullosa, Erosive lichen planus
- Immunological - Pemphigus vulgaris, P.vegetans, P.foliaceous
- Idiopathic - major apthous ulcer, minor apthous ulcer, herpetform ulcer
- Systemic - Pyostomatitis vegetans, Uremic stomatitis, Rhinosporidium, Haematological disease
- Neoplastic - Malignant ulcers
- Miscellaneous - Foliate papillitis, Necrotizing sialometaplasia.

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:: White lesions ::

White lesions are described as abnormal areas of the mucosa that appear whiter than the surrounding tissue and are usually raised, roughened or of different texture from adjacent tissue.

Classification :-

- Normal variants - Leukoedema , Fordyces granules, Linea alba
- Heriditary - Leukoedema, White spongy nevus, HBID, Dyskeratosis congenita
- Precancerous -
a) Precancerous Lesions: Leukoplakia, Erythroplakia, Bowen's disease, Actinic keratosis, Actinic chelitis
b) Precancerous Condition: Oral sub mucous fibrosis, Syphilis, Oral lichen planus, Dyskeratosis congenita, Lupus erythematous, Psoriasisis
- Skin diseases - White spongy nevus, HBID, Parakeratosis, Keratosis follicidans, Warty dyskeratosis, Psuedoxanthoma elasticum
- Systemic diseases - Uremic stomatitis, Diabetes stomatitis, Ulcerative stomatitis
- Infections - Oral hairy luekoplakia, Candidiasis, Parulis, Mucous patches
- Traumatic - Cheek biting, Frictional keratosis, Aspirin burn

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:: Red lesions ::

Red lesion is an area of reddened mucosa that may be smooth and atrophic looking or exhibits a granular,velvety texture.

Classification :-

1.Traumatic - Mechanical, Chemical and Thermal injuries
2.Infections -
a) Bacterial: Scarlet fever, Gingivostomatitis
b) Fungal: Erythematous candidiasis
c) Viral: Measles, Lymphonodular pharyngitis
3.Vascular - Haemangioma, Agranulocytosis
4.Dermatological - Pemphigus, Erythema multiforme, Erosive lichen planus, Lupus erythematosus
5.Systemic diseases - Uremic stomatitis, Ulcerative stomatitis, Diabetes, Scurvy, Pernicious anemia
6.Premalignant and malignant condition - Speckled leukoplakia, Erythroplakia, Systemic lupus erythematosus, Kaposi's sarcoma, Carcinoma in situ

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Condensing Osteitis

- Description:

It's a periapical inflammatory diseases, that results from reaction to infection, which is periodontal and not dental.
There would be bone production rather than bone destruction.

The most common site is near premolars and molars.
The Lesion appear as an radio-opacity in the periapical area hence the sclerotic reaction.
The sclerotic reaction result from good patient resistance and a low degree of virulence of the offending bacteria.
The associated tooth is carious or contains a large restoration.

- Synonyms:
1- Garre's Disease (described by Dr. Carl Garré in 1893).
2- Sclerosing Osteitis.

- Etiology:
Infection of periapical tissues of a high immunity host by organisms of low virulence.

- Treatment:
The offending tooth should be tested for vitality of the pulp, if inflamed or necrotic, then endodontic treatment is required, while hopeless teeth should be extracted.

- Prognosis:
if the offending tooth is extracted, the area of condensing osteitis may remain in the jaws indefinitely, and is termed osteosclerosis or bone scar.

- Differential Diagnosis:
1- Idiopathic osteosclerosis.
2- cementoblastoma.
NOTE: An abnormal result with pulp testing strongly suggests condensing osteitis and tends to rule out osteosclerosis and cementoblastoma.

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Denture Stomatitis (Denture Sore Mouth)

Definition:
- Denture-related stomatitis indicates an inflammatory process of the mucosa that bears a complete or partial removable dental appliance, typically a denture.
- It was known as: “chronic denture palatitis”, “stomatitis prothetica”, “denture related candidiasis” “denture-induced stomatitis” and “denture stomatitis”.
- The denture stomatitis occurs with patients of partial denture less than patients of complete denture.
- No racial or sex predilection exists.
- It can affect as many as 35-50% of persons who wear complete dentures.
- Denture sore mouth is common, but rarely sore.
- Caused mainly by a yeast (Candida) that is a normal inhabitant in the oral cavity, and it's not a transmitted disease.
- It can predispose to angular chelitis.
- It has no serious long-term consequences

Clinical Picture:
- Occurs in the maxilla more than the mandible, where the washing affect of salive is greater in the mandible.
- The Denture-induced stomatitis is assymptomatic, but patients may complain of halitosis, slight bleeding and swelling in the involved area, or a burning sensation, xerostomia, or taste alterations (dysgeusia).

Classification (Stages):
suggested by Newton in 1962, and states:
- Newton´s type I: pin-point hyperaemic lesions (localized simple inflammation)
- Newton´s type II: diffuse erythema confined to the mucosa contacting the denture (generalized simple inflammation)
- Newton´s type III: granular surface (inflamatory papillary hyperplasia)

Related disorders:
May be accompanied with other disorders of the same origin (Fungal), ex:
- Angular cheilitis
- Median rhomboid glossitis
- Candidal leukoplakia.

Aiteology:
The aetiology is best considered Multifactorial, but wearing the denture in the night is the major causitiva factor.
Other factors are:
1. Prosthetic factors:
- No denture stomatitis can exist without a prosthesis.
- Prosthetic traumatism is favoured by denture functional deficiencies

2. Infectious factors:
- The dentures can accumulate bacteria and yeasts, that cause the ecological changes:
- Bacteria proliferate: Staphylococcus species, Streptococcus species, Neisseria species, Fusobacterium species. or Bacteroides species has been identified in patients with denture stomatitis.
- Candida species, particularly Candida albicans, have been identified in most patients. Patients with denture stomatitis show higher intraoral concentrations of fungi than individuals without this disorder.

Predisposing factors:

1. Systemic factors
a. Physiological. (advanced age)
b. Endocrine dysfunctions.
c. Nutritional deficiencies.
d. Neoplasias.
e. Immunosuppression.
f. Ample spectrum antibiotics.

2. Local factors
a. Antimicrobials and topical or inhaled corticosteroids
b. Carbohydrate rich diet
c. Tobacco and alcohol consumption
d. Hyposalivation
e. Deficient oral hygiene
f. Wearing dentures (especially through the night)

Diagnosis:
- Clinical presentation of erythema and oedema on the palatal mucosa covered by the denture base (but not beyond) is a diagnostic finding.
- Take a smear of the palate to check for presence of Candida species, by staining with KOH, periodic acid-Schiff or by imprint cultures.
- Blood tests, microbiological studies or biopsy may be required.

Prevention:
• A routine basis inspection of the oral cavity for screening for this disorder, even when the lesions are asymptomatic.
• Properly denture sanitization and perform good oral hygiene
• Appropriate denture-wearing habits, instructing the patient to take his/her denture out of the mouth for 6-8 hours each day
• Patients with partial dentures should undergo periodic professional plaque control

Treatment:
• Good oral hygiene is mandatory.
• Local factors which promote growth of yeasts, such as smoking or wearing the dentures throughout the night, must be discouraged.
• Dentures should be removed for as long as possible and definitely overnight.
• Dentures should be brushed in warm, soapy water and soaked overnight in an antiseptic solution such as bleach, chlorhexidine or in any solution suitable for sterilizing baby´s feeding bottles.
• Denture fitting and occlusal balance should be checked to avoid trauma. A new prosthesis should be made, if necessary.
• Newton`s type I and II denture stomatitis have been successfully treated with low energy lasers to reduce inflammation of the supporting mucosa, Inflammatory papillary hyperplasia usually needs to be surgically removed before the denture is placed, and mild cases may respond to antifungal treatment.

• Antifungal medications are recommended when yeasts have been isolated, or when lesions do not resolve with hygiene instructions.

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Trismus

Introduction:

Trismus is a common presentation by the patient in routine dental practice. This condition causes difficulty in opening mouth which in turn impairs eating, interferes with oral hygiene, restricts access for dental procedures, and may adversely affect speech and facial appearance.

Trismus has number of potential causes and it’s important to recognize the underlying cause for effective management of this condition

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Definition:

Trismus in greek is Tonic contraction of the muscles of mastication.

The Normal Mouth Opening Range:
Range- 40-60 mm (avg-35mm)
Males display greater mouth opening

The Normal Lateral movement is 8-12 mm

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Causes Of Trismus (Etiology)

Several conditions may cause or predispose an individual to develop Trismus.

1. Intra-Articular Causes:

A- Ankylosis
B- Arthiritis Synovitis
C- Meniscus Pathology

Ankylosis:
- True Bony Ankylosis: can result from trauma to chin, infections and from prolonged immobilization following condylar fracture
Treatment- several surgical procedures are used to treat bony ankylosis, Eg: Gap arthroplasty using interpositional materials between the cut segments.

- Fibrous Ankylosis: usually results due to trauma and infection
Treatment- trismus appliances in conjunction with physical therapy.

Trismus Appliances:

Indications:
A- Intracapsular (TMJ) pathosis
B- Bony interferences from styloid or coronoid process
C- The presence of foreign body
D- Muscle fibrosis or immature scar tissue

Types Of Trismus Appliances:

A- Externally activated appliances
- Dynamic bite opener
- Threaded, tapered screw
- Screw type mouth gag
- Fingers
- Tongue blades
- Continuous-dynamic jaw extension apparatus.

B- Internally activated appliances

- Tongue blades
- Plastic tapered cylinder

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2. Extra-Articular Causes:

A- Infection
B- Dental treatment
C- Trauma

D- TMJ Disorders
E- Tumors and Oral care
F- Drug Therapy:
G- Radiotherapy and Chemotherapy
H- Congenital / Developmental Causes:
I- Miscellaneous disorders

A- Infection
Odontogenic- Pulpal
- Periodontal
- Pericoronal

Non-Odontogenic- Peritonsillar abscess
- Tetanus
- Meningitis
- Brain abscess
- Parotid abscess

The hallmark of a masticatory space infection is trismus. Or infection in anterior compartment of lateral pharyngeal space results in trismus. If these infections are unchecked, can spread to various facial spaces of the head & neck and lead to serious complications such as cervical cellulitis/ mediastinitis.
Treatment- Elimination of etiologic agent along with antibiotic coverage

Trismus or lock jaw due to masseter muscle spasm, can be a primary presenting symptom in tetanus, Caused by clostridium tetani, where tetanospasmin (toxin) is responsible for muscle spasms.
Prevention- primary immunization (DPT)

B- Trismus Related To Dental Procedure:
Oral surgical procedures- extraction of lower molar teeth may cause trismus as a result either of inflammation involving muscles of mastication or direct trauma to the TMJ
Inaccurate positioning of the needle when giving inferior alveolar nerve block before extraction
Barbing of needles at the time of injection followed by tissue damage on withdrawal of the barbed needle causes post-injection persistent paresthesia, trismus and paresis
Treatment- in acute phase
Heat therapy
Analgesics
A soft diet
Muscle relaxants (if necessary)
When acute phase is over the patient should be advised to initiate physiotherapy for opening and closing mouth.

C- Trauma:
Fractures, particularly those of the mandible and Fractures of zygomatic arch and zygomatic arch complex,Accidental incorporation of foreign bodies due to external traumatic injury
Treatment- fracture reduction, removal of foreign bodies with antibiotic coverage

D- TMJ Disorders:
Extra capsular disorders – myofacial pain
Intra capsular problems – disc displacement, arthritis, fibrosis etc
Acute closed locked conditions – displaced meniscus

E- Tumors And Oral Malignancies:
Rarely, trismus is a symptom of nasopharyngeal or infra temporal tumors/ fibrosis of temporalis tendon, when patient has limited mouth opening, always pre malignant conditions like oral sub mucous fibrosis (OSMF) should also be considered in differential diagnosis

F. Drug Therapy:
Succinyl choline, phenothiazines and tricyclic antidepressants causes trismus as a secondary effect. Trismus can be seen as an extra-pyramidal side-effect of metaclopromide, phenothiazines and other medications.

G. Radiology / Chemotherapy:

- Complications of Radiotherapy:
1. Osteoradionecrosis may result in pain, trismus, suppuration and occasionally a foul smelling wound.
2. When muscles of mastication are within the field of radiation, it leads to fibrosis and result in decreased mouth opening.
- Complications of Chemotherapy:

Oral mucosal cells have high growth rate and are susceptible to the toxic effects of chemotherapy, which lead to stomatitis.

H. Congenital / Developmental Causes:
Hypertrophy of coronoid process causes interference of coronoid against the anteromedial margin of the zygomatic arch.
Treatment-Roronoidectomy
Trismus-pseudo-camtodactyly syndrome is a rare combination of hand, foot and mouth abnormalities and trismus.

I. Miscellaneous disorders
- Hysteric patients: Through the mechanisms of conversion, the emotional conflict are converted into a physical symptom. Eg: trismus

- Scleroderma: A condition marked by edema and induration of the skin involving facial region can cause trismus

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Oral Herpes Simplex

Etiology:
Herpes virus hominis, Most commoly type I virus, but approximately 10% are thought to be caused by Type II.

Clinical Forms:
- Oral Herpes Simplex occurs in three clinical forms:
1- Recurrent small blisters on the lips commonly referred to as fever blisters or secondary herpes labialis. (most common form).
2- Generalized oral infection called primary herpetic stomatitis.
3- Small ulcers usually localized on palatal mucosa. (least common form).

Treatment:
- Antiviral drugs such as Acyclovir, Famciclovir, Penciclovir, Valacyclovir and over-the-counter Abreva have all shown that they can decrease the time of disease as well as help with pain management.
- Treatments that suppress the immune system abnormalities may improve more severe lesions and lessen pain.

Prognosis:
- Primary infection usually resolves in 10-14 days. Once the virus has entered the body, it travels through nerve trunks to the nearest ganglion where it may lie dormant for the remainder of the patient’s life.
- The Recurrence occured by “reawakening” of the virus, not reinfection from the outside.
Patients should drink liquids to prevent dehydration, should take a broad-spectrum antibiotic to control secondary bacterial infection, but does not shorten the viral infection. Antiviral drugs may shorten the duration of the disease if they are started early. (once the symptoms appear).
Clinicians should be aware that the herpes virus may cause disseminated infection including encephalitis in which case the prognosis is extremely grave.

Differential Diagnosis:
- Primary herpetic stomatitis may resemble oral lesions of erythema multiforme, but herpes can be diagnosed by exfoliative cytology.
- Lesions of herpangina and hand, foot and mouth disease, both caused by Coxsackievirus, may clinically resemble oral herpes virus infections.
- Recurrent intraoral herpes may be confused with herpes zoster.
- Aphthous Ulcer can be differentiated since it usually does not occur over bone, does not form vesicles and is not accompanied by fever or gingivitis.

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Aphthous Stomatitis

Description:
- This is one of the most common oral diseases.
- It's a painful lesion that size from less than 1 mm to 2 cm, single or multiple.
- There is three types: The small lesions are less than 0.5 cm and called the "Minor Aphthae", The large lesions are more than 0.5 cm and called the "Major Aphthae", while they may be Multiple and pinpoint seldom exceeding 1 mm and are called "Herpetiform Aphthae".
- The exact incidence is unknown, but estimates range from 20% to 60% of the population.
- The Lesion begins as a red macule, less often papule, but not blisted. Then it ulcerates and the ulcer become covered by pyogenic membrane producing the characteristic yellow-white center with surrounding erythematous flare.
- It's usually round to oval but may be elongated in natural folds such as the vestibule.
- The lips, cheeks, soft palate, floor of mouth, ventral and lateral tongue are often involved but attached gingival, hard palate and dorsal tongue are seldom affected.
(Occurs on freely movable mucosa that does not overlie bone).
- Aphthous lesions affect all age groups from young to old but young adults and females are more affected.
- Also Known as: Canker sores, recurrent aphthous stomatitis, RAS.

Etiology:
- The cause is unknown.
- There are too many theories for them all to be correct. Aphthous stomatitis may not be a single disease with a single cause but instead a variety of diseases all manifested by painful mouth sores.
- The concept that canker sores are caused by a microbiologic agent has been superceded by theories revolving around an immunopathogenesis. The deposition of antibodies and complement within epithelium and basement membrane during the early stages of the disease suggests a humoral immune response, and the influx of lymphocytes rather than neutrophils in early lesions points to a cellular immune reaction as well. It is yet to be learned if the immune response is directed against self (autoimmunity) or against an extrinsic antigen such as bacteria or viruses. To further cloud the issue, a variety of other factors have been implicated. Withdrawal of certain foods such as cheese, tomato products and gluten, as well as sodium lauryl sulfate-containing toothpastes, has been claimed to help some patients whereas in others, correction of iron, B12 and folate deficiencies have brought about a cure. Improvement of aphthous lesions during the last stages of pregnancy with exacerbation after delivery suggests that gonadal hormones may lay a role. The occurrence of canker sores during menstruation also suggests a hormonal basis. To add a final element of mystery, aphthous stomatitis has been reported to worsen when cigarette smoking is discontinued.

Treatment:
- To reduce pain, patients with few lesions may be treated with topical medications such as Orabase® with Benzocaine, Zilactin®, or Soothe-N-Seal®.
- Anti-inflammatory agents such as topical steroids or Aphthasol® have also been shown to be effective.
- For severe or widespread disease, systemic prednisone such as a Medrol 4 mg Dosepak® is helpful.
- Long-term systemic steroid therapy may be associated with numerous adverse effects, including osteoporosis, asceptic necrosis, cataracts, depression, fluid retention and exacerbation of diabetes.

Prognosis:
- Cure is seldom achieved but palliation and long-term remission may be achieved by above mentioned treatment.
- Without treatment, healing time varies from 4 days for a small lesion to a month or more for major aphthae.
- Major aphthae may also cause scarring.

Differential Diagnosis:
- Aphthous stomatitis must be differentiated from herpetic stomatitis, the disease with which it is most often confused.
- Recurrent intraoral herpes occurs almost exclusively on mucosa overlying bone. The hard palate is the most common site.
- Lesions indistinguishable from aphthous stomatitis have been reported in Behcet’s syndrome, Reiter’s syndrome, Crohn’s disease and celiac disease.

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Epulis fissuratum

 
- Description:
A Lesion that appears in the buccal vestibule of the anterior maxilla or the lingual aspect. (most commonly in anterior aspect)
Where the body of the dental prosthetic appliance flanges contact with for a long time, causing a two or more folds of soft tissue that is separated by a cental groove.
The excess tissue is firm and fibrous, and ulcerations may be present.
The size of the affected tissue varies widely, since almost the entire length of tissue around a denture can be affected.
Most of the patients are females (64% of cases study) in the fifth and sixth decade of like.
The lesion's duration is from one week to 10 days, but 40% of the patients reported a duration of 6 months to two years.
No symptoms are associated with the lesion except some pain with ulcerated types.
Also Known As: Granuloma fissuratum, inflammatory fibrous hyperplasia, denture epulis and denture induced fibrous hyperplasia.

- Etiology:
This is an inflammatory fibrous hyperplasia or oral mucosa caused by ill-fitting or over-extended denture borders.

- Histologically:
The excessive tissue is composed of cellular, inflamed fibrous connective tissue.

- Microscopic Appearance:
The appearance of an epulis fissuratum microscopically is an overgrowth of cells from the fibrous connective tissue. The epithelial cells are usually hyperkeratotic and irregular, hyperplastic rete ridges are often seen.

- Treatment:
Surgical excision of the lesion and reduction of the denture border.

- Prognosis:
Good

- Differential Diagnosis:
The lesion has such a characteristic clinical appearance that differential diagnosis is not a problem.
Persistent ulcerated areas in epulis fissuratum should be biopsied to rule out squamous carcinoma.
Folds similar to epulis fissuratum may be seen in Crohn’s disease.
Epulis fissuratum can also appear around dental implants. occurred because the Broken implant denture clasp with poor oral hygiene.

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Leukoedema

Definition:
It's a normal variation of the buccal mucosa, or inside surface of the cheek. It presents as a white-bluish tinge of the buccal mucosa but the color disappears when the cheek is stretched. This aids to differentiate this lesion from other similar looking conditions which could be premalignant, such as leukoplakia. It is more prevalent in people who have dark skin and can be more intense in smokers.

Etiology:
Intracellular edema of the superficial epithelial cells coupled with retention of superficial parakeratin is thought to account for the white appearance. Microscopic examination reveals superficial squamous cells have a clear, seemingly empty cytoplasm but it has not been shown that there is an increase in intracellular water. Thus, the term edema is questionable.

Histology:
The white appearance is caused by water within the spinous cells causing the light to reflect back as whitish.

Treatment:
None required.

Differential Diagnosis:
- White sponge nevus
- hereditary benign intraepithelial dyskeratosis
- dyskeratosis congenital...
All are extremely rare.

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Fordyce Granules

Description:
Fordyce granules appear as flat or elevated yellow plaques just beneath the mucosal surface. The most common site is buccal mucosa although they may be found anywhere in oral mucosa. Development of the oral glands parallels those of the skin, reaching maximum numbers at puberty. Eighty percent of the population are affected. The number of granules is quite variable. Fig. 1 illustrated a large number of granules on buccal mucosa.

Etiology:
They are normal sebaceous glands and considering they are found in approximately 80% of the population, should be considered normal anatomic structures.

Differential Diagnosis:
The clinical
appearance is characteristic

Prognosis:
Good

Treatment:
No treatment is required for Fordyce granules, except for cosmetic removal of labial lesions. Inflamed glands can be treated topically with clindamycin. When surgically excised, recurrence does not occur. Neoplastic transformation is very rare but has been reported.
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Eosinophilic Ulcer Of The Oral Mucosa

- Description:
Eosinophilic ulcer of the oral mucosa (also known as "Eosinophilic ulcer of the tongue," "Riga–Fede disease," and "Traumatic eosinophilic granuloma") is a condition characterized by an ulcer with an indurated and elevated border. The lesion might be tender, fast-growing and the patient often not be aware of any trauma in the area.

- Definition
Traumatic eosinophilic granuloma of the tongue (TEGT) is a reactive condition that commonly occurs on the ventral tongue.

 - Causes
It is often associated with trauma. However, other causes are suspected, such as drugs, inherent predisposition, immune reaction, or lymphoproliferative disorder.

- Differential Diagnosis
Squamouce Cell Carcinoma, Pyogenic granulomas, Lesions of a chronic granulomatous disease and Mesenchymal tumors

- Treatment
When the lesion is excised, recurrence often occurs. Palliative care with nonsteroidal anti-inflammatory drugs (NSAIDs) may be used, and topical steroids can be curative. If the lesion does not respond to treatment, biopsy is required.


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Osteoporotic Bone Marrow Defect

- Description:
It is a localized increase of hematopoietic bone marrow that creates a radiolucent radiographic defect.
They occur more commonly in women in the midyears and show a predilection for the molar region of the mandible.
They are especially common in extraction sites.
Scattered trabeculae may extend short distances into the defect or, in some instances, through it giving the defect a fairly characteristic appearance. Naturally there are no clinical symptoms.

- Etiology:
The etiology remains unknown.

- Treatment:
No treatment is required.

- Prognosis:
Good

- Differential Diagnosis:
This defect may easily be mistaken for a cyst or tumor. In those cases, Biopsy is required.

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Idiopathic Osteosclerosis

Definition:
Focal radiodensity of the jaw which is not inflammatory, dysplastic, neoplastic or a manifestation of a systemic disease.
It's an area of dense but normal bone in the jaws, which is usually painless and discovered by Routine Dental Radiographic Examination.

Description:
Osteosclerosis may occur anywhere in the jaws.
Most commonly, it appears to be attached to a tooth, specially around roots and inter-radicular.
The shape ranges from round to linear streaks to occasional angular forms.
They are more common in the mandibular molar-premolar area.
They are usually discovered on radiographs taken during the course routine dental care.
It appears in 5% of population, most commonly in the teen of 20s.

Etiology:
A reaction to past trauma or infection but it's difficult to rule out in some cases.

Treatment:
Because osteosclerosis is not a disease, no treatment is required. If there is doubt about the diagnosis, periodic X-rays are taken. Although some lesions may slowly enlarge, most remain
unchanged with time.

Prognosis:
Good

Differential Diagnosis:
Condensing osteitis, sclerosing osteomyelitis, cementoblastoma, hypercementosis.
Condensing osteitis may resemble idiopathic osteosclerosis, however, associated teeth are always
nonvital in condensing osteitis.

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