Sunday, July 31, 2011

Surgical Management of Cysts in Orofacial Region(Jaws)-Oral Surgery Lecture

CYST ENLARGEMENT
Cyst cannot stay at the same size. It will enlarge

3 THEORIES OF CYST ENLARGEMENT
(these theories might work together to cause enlargement)
  • Bone resorbing factor(theory 1)
The capsule of the cyst produce bone resorbing factors like Prostaglandins, Leukotrienes, osteoclast
  • Osmotic theory(theory 2)
The centre of the cyst has a higher concentration of sodium than the surrounding serum, so it tends to absorb water.
  • Hydrostatic pressure(theory 3)
This water that accumulates has hydrostatic pressure which probably stimulate the release of these factor, then these factor will resorb the bone. Eventually, the small sac will became bigger and bigger with time. The enlargement of cyst is slow, it’s not a rapid process that can take over months.

SYMPTOMS OF CYST
None.
  • Patient may be totally asymptomatic. The cyst does not cause much expansion yet.
  • Intraoral swelling
  • Extraoral swelling also possible
  • Intraoral discharge.
  • If the cystic sac manage to get outside the bone, then you will have discharge of straw-coloured or yellowish fluid from an intraoral sinus.
  • Secondary infection that will cause pain and abscess.
  • It is not painful, unless it get secondarily infection where you will have typical abscess like pain, tender teeth etc
  • Lower lip anesthesia which is rare.
  • A very big cyst that usually are infected will compress the inferior dental canal and mental nerve. But the most common cause of lower lip paresthesia is a tumor or osteomyelitis.
  • Difficulties with dentures.
  • The denture will not fit any more as it used to be
  • Movement or tilting of adjacent teeth.
  • A cyst locating between 2 roots, will cause the roots to move away from each other and the crown of each tooth will also move accordingly.
  • Facial asymmetry or swelling in one side.
  • But this rarely happens.
  • The best way to assess a swelling at the mid portion of the face is to look to the patient either from above or below, so that you can get better differentiation of normal and swollen side.
SIGNS
  • The signs are similar to the symptoms. The pt might be totally asymptomatic or will present with:
  • Swelling
  • Tender if become infected. Cysts are painless at the beginning. Pain only if it get infected
  • Expansion labio-bucally.
  • It is rare to have expansion lingually or palatally except the nasopalatine cyst. but cyst at the mandible will always have expansion labially or bucally. If you see lingual expansion, this is more likely to be a tumor rather than a cyst.
  • Sinus with straw-coloured fluid with shimmering cholesterol crystals
  • Displace teeth
  • Missing teeth
  • Pathological fracture (if the cyst was large).
  • A very large cyst can cause the bone to be so thin that might fractured easily by even a minor trauma.
  • This is a summary of time-scale FINDINGS when you try to palpate a cyst. When you examine a pt, you will only find one of these findings depends on at which stage the cyst are.



DIAGNOSIS

  • History and examination. This is very important
  • Radiograph (Intraoral Periapical, extraoral OPG). It is wise to have 2 radiograph that are right-angled to each other. Sometimes its good to have both intraoral PA and extraoral OPG to have an idea about the size or the extends of the cyst
  • Vitality test of the neighbouring teeth. This will tell you if the periapical area is the actual cause of the cyst (from a dead pulp that confirmed an inflammatory cyst)
  • Aspiration (with wide needle, no 18). This is very important when you are dealing with a jaw cyst. We don’t use fine needle to do aspiration of a cyst because it is for soft tissue masses, it will break when you try to enter a fine needle into a bone! You introduce the needle into the bone (insert the needle occlusally because this area usually thinner from the buccal or lingual area) and withdraw the content of this cyst.
  • Straw-coloured fluid and crystal (inflammatory cyst or dentigerous cyst)
  • If you put the fluid on a piece of gauze, you can see some spots in the yelow clear fluid. The spots that appear like sugar or salt is the cholesterol crystals. When you put it under the sunlight, you can see the cholesterol crystals clearly (shimmering).
  • Blood hemorrhagic (small amount of blood most probably a hemorrhagic bone cyst. But if you have a mass bleeding once you insert the needle and the syringe filled with blood spontaneously, this is hemangioma osteomyelitis.
  • Thick creamy fluid (keratocyst)
  • Air (maxillary sinus, hemorrhagic). There is condenstion of air in the syringe
  • Nothing (tumor). You will have negative pressure in the syringe. When you leave the plugger, it will go back by itself. This means you are dealing with a soft tissue mass that most probably a tumor, until proven otherwise.
  • To minimize the amount of pt’s unease, it is wise to put 2 needles; one for the entry of the air (needle without syringe), while the other one (needle with syringe) for the aspiration. Otherwise it’ll become painful during the withdrawal.
  • (like when you want to open a can, you’ll do 2 holes for the content to come out easily. It’s physics.)
  • Soluble protein (albumins and globulins) determintion of the aspirate (electrophoresis)
  • 5-10g/dl: inflammatory cyst (range of serum soluble protein)
  • <4g/dl   : keratocyst
  • Biopsy (incisional or excisional). For a confirmation of your diagnosis or if you have no clue at all, do a biopsy. We can do excisional biopsy if the cyst was small. For a very big cyst, do a flap, take some of the cyst (incisional) and send it to the histopahology lab.

TREATMENT
Once we have establish the diagnosis, we can go on to the treatment. Firstly we need to tell the pt that it is a cyst. It is benign, will not metastasize or kill the pt. That’s why some people ask why we cannot just leave it? This is because they will enlarge, bone expansion and pathological fracture. The cyst also can get infected. That’s why the pt need treatment.
Preoperatively
Vitality test on the teeth that had been reached by the cyst
Root filling of non-vital teeth
Let’s say we have a big periapical cyst at the upper lateral incisor. It might be associated with lateral incisor but in the x-ray you can see the cyst had gone to periapical of the central, the canine and also the 1st PM. During surgery, we will remove the cyst, and do apisectomy of the involved tooth. If we know by vitality test that the central, canine and 1st PM are vital, we will not do anything on that teeth. we will not disturb the vessels that inserted into the foramina of the vital teeth. That’s why it is important to do vitality testing before any surgery.

Treatment modalities
  • Marsupialization : opening a window
  • Enucleation : complete removal of the cystic sac
After done with enucleation, we can either primarily close it (suture the flap).
*in americam school they will do bone graft before suturing but we from british school won’t*
*If the cyst get infected, we will leave it open. Put a tag and it will heal by itself (not used anymore)*
  • Decompression (Marsupialization followed by Enucleation)
Post-operatively
Antiseptick pack
obturator

MARSUPIALIZATION
To undertsand marsupialization, imagine the lecture room as a cyst and outside it is the oral cavity. The wallpaper that lining the room is the cystic lining. After we open the door (do surgery to open the cyst), we will suture the cystic lining (the wallpaper of lecture room) with the oral cavity lining (wallpaper outside the lecture room) and then leave it to heal. What happened was we had converted the cyst into a small pouch of the oral cavity. This action of maintaning an open window will cause the cyst to be fluid free and contain zero pressure. So bone will start forming outside the cyst and causes the cyst to shrink with time. Eventually, it will be filled completely with bone and the whole cyst will disappear. 
So for marsupialization to succeed, we need to maintain the window open. How? By constructing a small denture or obturator (something to obturate the opening) that fit inside the opening that you had created. The pt need to clean this obturator after every meal and put it back to keep the pouch open, preventing any food or fluid to accumulate inside the cyst that might cause secondary infection.
If you have no hydrostatic and osmotic pressure, the cyst will not enlarge. Think like it’s a battle of the bone-forming power and the bone-resorbing power of the cyst. If you weaken the cyst, the bone-forming power will win!
What if we just aspirate the fluid inside the cyst, without opening any window? The answer is, the fluid will start forming again because of the osmotic theory. So the idea of marsupialization was to open a window, making a zero pressure area.
This is an example of a cyst that is compressing the mental nerve. Removal of the cystic lining might danger the mental nerve and the pt will have lower lip numbness. In this situation, its better to do marsupialization.
Open a window by raising a flap.
Remove some bone that covering the cyst. Just a small window, not need to remove the whole bone covering the cyst.
Remove the impacted tooth that causing the dentigerous cyst.  
At the end, the mandible is hollow. This yellowish tissue is the lining of the cyst. We will suture it with the lining of the oral mucosa.
To maintain the area open, fill the pouch with an antiseptic pack
construct an obturator (for sure you need to take an impression first. The obturator is out of occlusion)

How about if we are dealing with dentigerous cyst? The impacted teeth that was the main factor of the cyst, when we do marsupialization, the teeth will move with the shrinken cyst.  Impacted teeth are very dramatic, they can move within the bone.
The aim of marsupialization is to gain bone. For example in a case where we have a very thin bone around the cyst (usually at the mandible), surgery might fracture the bone. so by doing marsupialization, bone will form by time. We can either wait for the complete bone formation in the pouch which will took about 6 months (in this case we do marsipulization only) or we can do enucleation after we are sure that the bone are thick enough to receive a surgery (in this case, we do decompression).
This methode also apply when we have a cyst compressing a nerve. After few months of marsupialization, the cyst will shrink away from the bone and we can consider doing enucliation at this time without damaging the nerve.
Advantage
Disadvantage
Indication
Simple (not necessarily need a specialist)
Avoid damaging nerves
Avoid pathological fracture
Leaves pathological tissue
(We cannot sure whether it is a cyst or a cystic tumor.
There might be a small tumor that we do not reach during biopsy. This is potentially dangerous)
Needs great compliance (pt need to wear obturator for long periods of time)
Incovenience for patient
Hygiene demands
(bad OH can cause bad smell of the mouth)
Very large cyst near vital structure
Patient unfit for surgery (poor medical status)
Infected cyst
(in infected cyst, the lining is friable. Enucliation will cause the lining to tear and we might leave a small piece of the cyst. A remaining cyst can cause recurrence)

ENUCLIATION
Enucleation means complete removal of a cyst. This can be done by currettage (using currette),or by blind sections of cystic lining (we put a blunt instrument and you sort of ‘peeling’ the bony lining).
For a cyst that has a recurrence potential, you need to do peripheral osteoctomy after removing the cyst. How? By removing the 3-4mm of bone surrounding the cavity with a big, sharp bur. Make sure that the bur are big enough to remove any remaining cyst or daughter cyst (if dealing with keratocyst). 
Opening a wide flap or window and remove all the cyst as one sac(with the lining intact). Then we close the window and leave it to be fill up with bone over time.
In the case of dentigerous cyst, when you open the area you can see a bluish sac which is the cyst. Then you need to enlarge the bone around it. You bluntly remove the whole cyst with the causative impacted tooth. You can see that this is obviously a dentigerous cyst because the crown was completely covered with the dentigerous sac. 

Advantage
Disadvantage
Contraindication
Remove all pathological tissue
Little patient compliance
-It just takes about 10 days to see any healing activity.
-oral hygiene is not so important.
-You can just leave the patient and do follow-up
Difficult
-You need a specialist to do especially if the cyst was too big or the cyst in the maxilla near the orbit or pterygomandibular area. You need to have experties.
High morbidity to surrounding tissue
-that’s why you need to trim some bone so that you can get the whole cyst out
-you might endanger the maxillary sinus, the nasal lining of the nose, the ID canal
-you might also thinning the posterior or the lower border of the mandible, making it susceptible to fracture

In most cases we use this methode. We just do marsupialization in cases that we had discussed.
Large cyst encroaching vital structure
Existing pathological fracture
-pt come with already fractured bone because of the large cyst. In this case it’s contradict to do enucleation. We will do marsupialozation with splinting of the fractured bone.
-We can consider doing enucleation after we gain some bone

DECOMPRESSION
As we has discuss previously, usually we do marsupialization first.
Continue with enucleation after we had:
gain some bone (bone deposition)
the cyst has become smaller
the cyst has move away from important sturucture (ID canal, maxillary sinus)
Indication:
Very large keratocyst
In this case we have save the patient from removing the mandible. I think it is not ethical and inhumane to resect the mandible only bacause of a benign cyst.
There are some authorities (mostly the non-dental authorities like ENT specialist and plastic surgeon) saying that we can resect the mandible because of the large keratocyst. But I think we need to have some patience to wait and allow the cyst to shrink. It’s a different story if we are dealing with a tumor but a keratocyst is not indicated for bone resectomy.

Cystic variants of ameloblastoma

Dentigerous cyst
In case of dentigerous cyst, after we’re done with marsupialization, the tooth will move with the shrinken cyst. if the tooth has good eruption potential, it will erupt at It’s normal position. But in majority if cases, the impacted tooth has bad eruption potential. In this situation we need to remove the impacted canine with the cyst at the same time.
Eruption cyst
Eruption cyst is easy to treat. You just de-roof it, excise the bone and the tissue covering the cyst (go down until you found the cavity of the cyst). Once you remove the tissue and bone, you will see the crown of the erupting tooth in the cystic cavity. Then we just leave it because the tooth  will erupt and the whole thing will heal.
Solitary bone cyst
You open the area, you might do detachment or do not. it will heal once you open it. Nobody knows why, but if you open the area, induce some bleeding inside it and it will heal.
Keratocyst
We know that it has high recurrence rate.
4 theories of high recurrence rate of keratocyst:
The cyst stays in marrow spaces. Marrow spaces have trabeculaetion. When you try to remove it, you might leave some remnants of cyst in it.
This lining is friable and it might tear during enucleation where we might leave some remnants.
formation of daughter cyst either as capsules or within the surrounding bone
the epithelial lining of keratocyst has growth potential
If you see in Dentigerous cyst you have stacking of cyst over  each other. While if u look at keratocyst you can see that there is definite stratification of the epithelial layer of the keratocyst (the stratification was very similar that you see at the skin). It is a tissue, not only collection of cells. It have potential of growth at the base and it will move upward until it reaches the keratinized area and became ortho or parakeratinized as we mention in the last lecture.
Because of this growth potential, it is most probably why the keratocyst recur. They behave like tumor that they can grow independently without depending on hydrostatic pressure only.
Treatment is either by enucleation but u have to eliminate the daughter cyst by peripheral osteoctomy and you have to use the big bur. If you want to gain mandible      
Some authorities do en block resection. They will resect the cyst 1cm in front, behind and below the bone. it leaves a big cavity in the mandible. And if it’s already big, they will do total  jaw resection (maxillectomy or mandibulectomy). But we don’t do this.

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Concept of Neutral Zone in Prosthodontics-Power Point Presentation(PPT) Free Download

Concept of Neutral Zone in Prosthodontics-Contents
  • Importance of Neutral Zone
  • The Neutral Zone Philosophy
  • Muscles involved in Neutral Zone
  • Techniques of location of Neutral Zone
  • Recording Neutral Zone for a Single Complete Denture


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Concept of Neutral Zone in Prosthodontics PPT

Saturday, July 30, 2011

Short notes on Important Diseases of Mouth, Salivary glands & Oesophagus


Oral Cavity

Congenital development disorders

Fordyce’s spots: Numerous yellowish white bodies found on the upper lip as a result of ectopic sebaceous glands.

Lymphoepithelial cyst: Can occur anywhere (i.e.: oral, cervical etc). It’s a cyst whose internal lining is keratinised squamous epithelium, and its outside is lined by a capsule. Within this cyst are multi-lymphoid follicles which contain lymphocytes.

Peutz-Jeghers syndrome: Intestines have hamartomatous polyps, and this is associated with brown black lesions around lips.

Macroglossia: big tongue. You get this if you have three copies of chromosome 21, instead of the normal two.

Microglossia: small tongue. 

Cleft upper lip (hare lip) + or - cleft palate: Cleft palate affects roof of the mouth.

Ankyloglossia: The fraenulum underneath your tongue attaches the tongue to the base of the oral cavity, thus limiting its movement. If you have a very short fraenulum or it consolidates, it limits tongue movement - tongue tie.

Branchial cleft cysts: There are lumps on one side of the neck, which contains fluid. Abnormal development of neck structures.

Xeroderma Pigmentosa: Inherently, the body can repair DNA damaged from UV rays. In this condition, which is inherited, the body is not able to do this. The DNA of skin cells are damaged permanently. It is autosomal recessive (i.e.: need two recessive genes for trait to be seen).

Oral inflammations

Lichen planus: inflammatory condition of the skin. No cause indentified, but allergic reactions that look similar have been identified after use of drugs. It is not infectious or cancerous.

Aphthous ulceration: Round/Oval ulcers on mucous membranes that are not firmly bound to bone. Common areas are: inside of lips, insider of oral cavity, genital areas etc.

Oral candidiasis (aka: thrush, moniliasis, candidiasis): Predominantly caused by candida albicans. Its is a commensal in 30-40% of humans, and commonly affects the oral cavity. Clinically, you see creamy blotches insider oral cavity or tongue. It is an opportunistic infection, which can occur if certain predisposing factors exist: 1) antibiotic treatment, 2) diabetes mellitus, 3) immunocompromised, 4) debilitation.


Other oral conditions
Crohn’s disease: This is an inflammatory bowel condition. Ulcerative colitis is the other variety. Crohn’s can affect any part of the GIT system. See other lectures for more information.

Dilantin therapy: Fibrous hyperplasia of the gingiva can occur with this therapy.

Amyloidosis of tongue: Amyloidosis is basically deposition of proteinatious material called amyloid in the extracellular tissue of organs. In this case, these deposits occur in the tongue.

Leukoplakia & Erythroplasia (erythroplakia)

Leukoplakia: This affects the oral cavity. Patient notice a white patch that is at least 5cm in diameter, and it cannot be rubbed off and not be diagnosed as anything else. It is potentially (i.e.: different types of leukoplakia have different rates of progressiont to cancer) a pre-cancerous lesion.

Erythroplasia: This is basically a red patch/plaque that cannot be categorised as any other disease process. This is also a premalignant lesion.

Premalignant lesions

Tumours of Oral Cavity

Benign lesions
The most common type of benign lesion of oral cavity is: squamous papilloma. It contains core of connective tissue, surrounded by glandular proliferation of mucosa.

Squamous cell carcinoma
This is the commonest tumour of oral cavity. Commonly occurs in older people. Basically, there is abnormal proliferation of mucosal cells. Can involve specifically the: lip, dorsum of tongue, palate. Predisposing factors: tobacco, alcohol, betel nutes (Asians), UV light. Infections such as: candidiasis, human papilloma virus, herpes simplex virus can also lead to squamous cell carcinoma. Premalignant lesions (described in lecture notes) n the vicinity of oral cavity can also lead to this. Histological patterns: moderately differentiated mucosal cells proliferate into submucosa layers, sometimes can be into lumen (exophytic). Then spreads to muscle and regional lymph nodes.
Other malignant neoplasms
Adenocarcinoma / adenosquamous carcinoma of oral cavity, connective tissue neoplasms, malignant melanoma.

Salivary glands

Disorders of secretion

Xerostomia (i.e.: dry mouth): This is a symptom of several diseases. Causes can be: medications (i.e.: antihypertensive, antidepressant, analgesics, diuretics, transhistamines), stress/fear/anxiety, Sjiogren’s syndrome (dry eyes + mouth) – causes fibrotic glands, irradiation sialadenitis (loss of secretory cells).

Sialorrheoa (ptyalism): increased salivary flow. Cause: neurological, acute inflammation of oral cavity.

Salivary calculi: Stones in the salivary glands (i.e.: submandibular & parotids, not sublingual) or salivary ducts (i.e.: submandibular & parotids). M:F = 2:1. Most common beyond 2nd decade of life.

Salivary cysts: Three types à 1) mucous extravasation (too much production), 2) mucous retention (blockage in ducts), 3) ranula (similar to 1&2)

Inflammatory disorders

Acute sialadenitis (inflammation of salivary gland): inflammation most often affects parotid gland (CT scan shows enlarged parotids). Usually caused by bacterial infections due to dehydration of oral cavity (xerostomia). Causative organisms: Strep viridans, Staoh aureus.

Chronic sialadenitis (as above): This occurs chronically due to unresolved acute sialadenitis, or due to strictures or stones. Eventually, inflammation leads to fibrosis of salivary gland.

Chronic recurrent parotitis: Clinically, you get tender parotid glands during GI examination. Usually seen in children and female adults. The parotid ducts are proliferating & dilated, and you get acinar atrophy and fibrosis.

Specific bacterial and granulomatous lesions: GATSS.

Viral infections: CM

Sjogren’s syndrome

This is characterised by dry eyes (keratoconjunctivitis sicca) and dry mouth (xerostomia). It occurs because the lacrimal and salivary glands are attacked by lymphocytic and other immune cells. 90% are F > 50yrs. Commonly associated with Rheumatoid arthritis, SLE & scleroderma.

Tumours of salivary gland
There is a whole heap. Refer to lecture notes. Just remember the basic sequence: adenoma, carcinoma, non epithelial tumours, malignant lymphomas, 2nd tumours, unclassified tumours, tumour like conditions. I doubt we need to know all this. If so, it’s ridiculous!

Oesophagus

Congenital and development disorders

Heterotopias: This is any deviation of any organ from its natural position.

Congenital cysts + duplications: Cysts might develop within wall of the oesophagus. Essentially, they can impinge on the lumen of the oesophagus, causing problems in the passage of food.

Oesophageal atresia: congenital closure of the oesophagus.
Oesophageal fistula: connections between oesaphus - trachea/bronchi. Food enters the lung, and air enters the oesophagus. Major problems.

Oesophageal webs/rings: congenital narrowing - Dysphagia.

Functional disorders

Achalasia: Basically, the lower oesophageal sphincter fails to open during the food passage process. This is because of neurogenic failure (i.e.: defective relaxation, or increased resting tone of sphincter muscle). Therefore you have mega-oesophagus (2nd year notes).

Mallory Weiss Syndrome: This is a longitudinal tear in the oesophagus at the esophagogastric junction. Associated with: chronic cough, straining at stool, severe hiccups, vomiting and gastric reflux (alcoholism).

Diverticula: Outpouching of the ailementary tract. Can occur in the oesophagus. HIstologically, outpouching contains all visceral layers (mucosa, submucosa, muscularis mucosa, serosa). Three areas: Zenker, Traction, Epiphrenic.

Inflammations – oesophagitis

Reflux oesophagitis: Risk factors: smoking, hiatus hernia, obesity, drugs, duodenal ulcer. Patterns: 1) Reflux, 2) Erosive / ulcerative, 3) Peptic stricture, 4) Barret’s. 1): gastric contents reflux into the lower oesophagus, 2) erosion of the mucosa due to some other factor other than gastric contents, 3) if there is narrowing of the stomach, then stomach contents will back up and flow into the oesophagus, with help from defective LES. Histopathology: 1) usually basal zone contains squamous epithelial cells that are yet to move into the top zones. In oesophagitis, you see more 20% of the epithelium devoted to this region due to high turnover of cells from destruction. 2) elongation of lamina propria papillae, 3) inflammatory cells present in epithelium: eosinophils, neutrophils, lymphocytes.

Barrett’s oesophagus: This occurs when there is prolonged gastric reflux injury to the oesophagus. The squamous cells are replaced by metaplastic columnar cells (more resistant to acid injury). It resembles gastric mucosa rather than oesophageal mucosa. Histopathology: Three types of mucosa have been described. 1) gastric fundic type mucosa with chief and parietal cells. 2) mucosa resembling the cardia region (more mucous cells), 3) intestinal mucosa with villi and goblet cells. Should search for any dysplasia in the histological section - prevent malignancy. Look for nuclei in the basal aspect of epithelial cell (low grade dysplasia), or apical aspect (high grade dysplasia).

Other causes of oesophagitis: 1) ingestion of mucosal irritants (i.e.: alcohol, corrosive agents, alkaline agents, smoking, excessive hot foods), 2) anticancer therapy that is toxic to tumour cells (i.e.: may also affect normal cells), 3) infection: bacteraemia/viraemia (HSV, CMV), 4) fungal infections: candidiasis, 5) uraemia (setting of renal failure).

Other conditions

Oesophageal varices: This is caused due to increased pressure in the oesophageal veins causing dilated, tortous veins - varices. Associated with alcoholic cirrhosis. The reason for dilated tortous veins is because of portal hypertension. Increase pressure causes the systemic circulation to take up the venous blood (i.e.: oesophageal veins are key area of portal-caval anastomoses).

Hiatus hernia: This is caused by the widening of the space between the muscular crus of the diaphragm and the oesophageal wall. This causes the stomach to herniate through the oesophageal hiatus.

Tumours of the oesophagus -

Benign tumours

These tumours of the oesophagus are mesenchymal in origin and lie within the oesophageal wall. Most common are tumours of the smooth muscle of the oesophageal wall - leiomyomas. Polyps can also occur. If polyps contains lipid material - lipoma. If they contain vascular material - vascular polyps. Squamous papilloma can also occur. Benign tumours of the nerves - neurofibroma and all can also occur.

Malignant tumours

Most commonly squamous cell carcinoma & adenocarcinoma of the oesophagus. Secondary tumours can also occur. Other tumours are rare and can occur, such as: malignant melanoma, carcino-sarcoma, adenoid cystic carcinoma.

Squamous cell carcinoma

Risk factors: Male>Female, Alcohol, Tobacco, prolonged oesophagitis, Barett’s oesophagitis, Dietary factors: food carcinogens combined with nutritional deficiencies. Genetic component is not really that great.

Location: 50% - middle 1/3, 30% – lower 1/3, 20% - upper 1/3.

Patterns of growth: Three types seen, 1) protruded (60%) – lesion is exophytic and protrudes into the lumen, 2) diffuse infiltration of the oesophageal wall and no where else. This causes thickening, rigidity and narrowing of lumen. 3) excavated lesions where the cancer becomes necrotic and ulcerates through the oesophageal wall, and may even penetrate into the respiratory tree or aorta.

Adenocarcinomas

Common in lower 1/3 of the oesophageal and associated with Barrett’s mucosa. Histopathology: Microscopically, most tumours are mucin producing and glandular. 


Orthodontic Treatment Planning

  • The treatment planning approach advocated here is specifically designed to avoid both missed opportunities (the false negatives or under-treatment side of treatment planning) and excessive treatment (the false positive or over-treatment side), while appropriately involving the patient in the planning.

1.  The sequence of steps in planning orthodontic treatment
- Diagnosis results in a comprehensive list of the patients problems.
  1. Separate orthodontic (developmental) problems from pathological ones.
  2. Put the orthodontic problems in priority order.
  3. Note the treatment possibilities, being sure to be complete.
  4. Evaluate the possible solutions, considering factors that can affect the probable result.
  5. Establish the treatment plan concept in an interactive session with the patient and parents.
  6. Develop the detailed plan of clinical steps and procedures.

  • Control all disease states first
  • Setting priorities for orthodontic treatment
  • Balance between patient’s wishes and the severity of the problem
  • Above all do no harm

a) Creating the Problem List:  Pathologic vs. Developmental Problems
An important principle is that a patient does not have to be in perfect health to have orthodontic treatment, but any problems related to disease and pathology must be under control.  Developmental problems should be identified.
b)  Setting Priorities for the Orthodontic Problem List
Putting the patient’s orthodontic (developmental) problems in priority order is the most important step in the entire treatment planning process.  In order to maximize benefit to the patient, the most important problems must be identified, and the treatment plan must focus on what is important for that particular patient.  Sequence the 5 components of the Ackerman-Proffit scheme based on severity

2.  Treatment Possibilities
At this stage each problem is considered individually, and for the moment the possible solutions are examined as if this problem were the only one the patient had.  Broad possibilities, not details of treatment procedures, are what is sought.  The objective is to be sure that no reasonable possibilities are overlooked.
Factors in evaluating treatment possibilities
a)  Interaction among possible solutions – example: relation between horizontal and vertical dimensions
b)  Compromise:  In a broad sense, the major goals of orthodontic treatment are ideal occlusion, ideal facial esthetics, and ideal stability of result.  Often it is impossible to maximize all three. An example of compromise is extraction of teeth for orthodontics
c)  Cost-risk/ Benefit analysis:  Often Cost-Risks of procedures are overlooked in the light of benefits.  “Is it worth it?”  Benefits need to outweigh the cost-risks.  Costs include “burden of care”.  Risks include negative consequences, side effects, and unexpected events.

3.  Informed Consent
·           Paternalistic approach:  the doctor should analyze the pts  situation and should prescribe what he or she had determined to be the best treatment – the doctor, as a father figure, knows best and makes decisions (No longer used)
·           Patient centered approach:  pts have a right to determine what is done to them in treatment. Pts must be told what their problems are, what the treatment alternatives are, and what the possible outcomes of treatment or no treatment are likely to be.

4.  Indication for Orthodontic Treatment
a)  Psychosocial (treat only if severe malocclusion)
b)  Developmental (ankylosis, or congenitally missing teeth)
c)  Functional (respiration, TMD, Mastication, Speech)
d)  Trauma/Disease control (tx for prevention of trauma to protruding incisors, tx not indicated for disease control in kids)

5.  Timing of Orthodontic Treatment
a)  Traditional timing during adolescent growth spurt and permanent dentition
b)  Treatment in the mixed dentition

6.  Treatment in the primary dentition – summary
·           Malposed, crowded, and irregular incisors are uncommon, but the absence of spaces between primary incisors often indicates that there will be crowding when permanent incisors erupt.  No treatment is indicated until the mixed dentition.
·           Space should be mnaintained for missing primary molars, but not anterior teeth.
·           Posterior crossbites, particularly those with a lateral shift of the mandible upon closure, should be treated in the primary dentition, either by occlusal adjustment or by maxillary expansion.
·           Anterior crossbites caused by forward mandibular shift should also be treated early
·           Although skeletal anteroposterior and vertical problems can be detected in the primary dentition, treatment is indicated only for the most severe problems.

7.  Treatment in the early mixed dentition
a)  Moderate problems
Space problems (missing teeth, localized space, generalized moderate crowding)
Irregular/Malpositioned Incisors (spaced and flared max incisors, max midline diastema, anterior crossbite)
            Posterior Crossbite
            Anterior Open bite
            Over retained Primary teeth and Ectopic Eruption
b)  Severe problems – focus on “Serial Extraction”
                        Skeletal
                        Dentofacial Problems related to incisor Protrusion
                        Space Discrepancies of 5mm or more
                        Serial Extraction
·           Applies to pts who meet the following criteria: 
1.      no skeletal disproportions
2.      class I molar relationship
3.      normal overbite
4.      large arch perimeter deficiency (10mm or more)
·               Procedure consists of 4 steps
1.      Extraction of primary lateral incisors as the permanent central incisors erupt (if necessary, often happens naturally)
2.      Extraction of primary canines as the permanent laterals erupt
3.      Extraction of primary fist molars, usually 6 to 12 months before their normal exfoliation, at the point when the underlying premolars have one half to two thirds of their roots formed
4.      Extraction of the permanent first premolars before eruption of the permanent canines.

8.  Treatment for Adolescents (Late mixed and early permanent dentition)
Dental Component
Late Mixed Dentition
Early Permanent Dentition
Alignment Problems
Spacing = no tx ??
Crowding & protrusion= serial extraction/space maintenance with appliances
Crowding: orthodontic appliances
interproximal reduction/Extraction
Spacing:  retraction/Restorative options
Transverse Problems
Excess = Constrict dental archform
Deficiency = Expand dental archform (RPE, fixed or removable appliances)
Excess = Constrict dental archform
Deficiency = Expand dental archform
Severe: surgery
Anteroposterior Problems
Camouflage
Growth Modification

Distalize or Advance Teeth
Camouflage
Surgery
Vertical Problems
Excess = Intrude teeth
Deficiency = Extrude teeth
Growth modification
Excess = Intrude teeth
Deficiency = Extrude teeth

Skeletal Component
Growing (Late Mixed Dentition)
Non-Growing(Early Permanent)
Alignment Problems


Mild:  Camouflage ??
Severe:  Surgery ??
Transverse Problems
Excess = No Treatment
Deficiency = RPE (max)/No Tx (man)
Mild:  Camouflage
Severe:  Surgery
Anteroposterior Problems
Excess = HG (max)/No tx (man)
Deficiency = Functional Appliances
Mild:  Camouflage
Severe:  Surgery
Vertical Problems
Excess = Functional Appliance
Deficiency = Functional Appliances
Mild:  Camouflage
Severe:  Surgery
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