Minggu, 31 Juli 2011

Polymers Used in Prosthetic Dentistry-Dental Materials Lecture Note

  • Polymer is a molecule that is made up of many units.
  • Oligomer is a short polymer composed of two, three, or four mer( mer = unit) units.
  • Monomers  (mono= single) are the molecules that unite to form a polymer, and the process by which this occurs is termed polymerization.If monomers of two  or more different                   
  • types are joined, copolymers are formed.Copolymers  may be either random(mers do not appear in specific order) or block (large numbers of one type of mer appear arranged in sequence).Atoms along the length of any polymer are joined through strong, primary covalent bonds.
  • There are three basic spatial structures of polymers: linear, branched, and cross- linked.
  • Linear and branched molecules are discrete but are bonded to one another through weak, physical bonds.Upon heating, the weak bonds break and the ability of the chains to then slide past one another results in a softened material.Upon cooling, the bonds reform and hardening occurs.Materials that are able to undergo this process are termed thermoplastic (polyvinylacrylics, poly(methyl methacrylate)).
  • Cross- linking results in the  formation of a network structure of covalently bonded atoms;primary linkages occur between chains, and the polymer actually becomes a single giant macromolecule.The spatial structure that allows chain sliding upon haeting is not present in cross- linked  materials.cross- linked polymers therefore do not undergo softening upon heating and are termed thermosets (sylicones, cross-linked poly(methyl methacrylate), bisphenol A-diacrylate,cis-polyisoprene).
  • Longer chains and higher molecular  weight result in the polymer‘s increased strength, hardness, stiffness, resistance to creep along with increased brittleness.Small plasticizer molecules, when added to a stiff uncross-linked polymer, reduce its rigidity.When small molecules surround large ones, the large molecules are able to move more easily.A plasticizer therefore lowers the glass-transition temperature of the polymer,so a material that is normally rigid at a particular temperature may become more flexible.The glass-transition temperature is the temperature at which a polymer ceases to be glassy and brittle and becomes rubberlike.


  • There are two types of polymerization reactions: additional polymerization, in which no by- product is formed, and condensation polymerization, in which low molecular weight by- product such as water or alcohol is formed.Polymerization has four stages: activation, initiation, propagation, termination.Reaction may be accelerated by light, heat, radiation or small amount of peroxides.Free radical additional polymerization is used for the synthesis of polymers.The free radicals are produced by reactive agents called initiators.The most popular initiator is benzoyl peroxide.Activation-involves decomposition of the peroxide initiatior using special conditions.Initiation-involves production of free radicals, which will encourage a polymer chain to begin growing.Activator allows polymerization to occur at low temperature(aromatic tertiary amines).
  • Free- radical molecules have chemical groups with unshared electrones.In chemically activated systems, free radicals are produced by the reaction of an organic poroxide initiator and amine accelerator.In light- activated systems, the  scission of camphorquinone results in the production of two molecules with one production, the free radicals attack the double bonds of available monomer molecules, resulting in the shift of the unshered electron to the end of the monomer and the formation of activated monomer molecules.Propagation- Activated monomers attack the double bonds of additional available monomers, resulting the rapid addition of monomer molecules to the free radical.This stage continues as the chain grows and length.Termination-it is posible for the propagation to continue until the supply of monomer molecules is exhausted.These reactions produce dead polymer chains which are not capable of further additions.Small amounts of inhibitors, such as hydroquinone, may be added to the monomer to increase storage life.Hydroquinones react with free radicals, thereby decreasing the rate of initiation.

Classification of denture base, liners and tissue conditioners:

Denture base:

I. Heat –cured (PMMA )

  1. conventional            
  • Unfilled
  • Re-inforced (Carbon,Polyfiber)
    2.high impact

II. Autopolymerized(PMMA)

III.Injection molded  1.  PMMA polycarbonate nylon

Soft liners:   

I. Acrylic

II.silicone      a)  room temperature vulcanizing (RTV) heat cured

Tissue conditioners-

plasticized acrylics

Denture base polymers

The polymeric denture base can consist of either a simple stiff base on which the teeth are arranged, or a sandwich of stiff base and a resilient liner to provide greater retention and comfort.When the tissue underlying a loose denture is traumatized due to the constant motion of the hard plastic over the mucosa, a viscoelastic gel known as a tissue conditioner can be molded onto the fitting surface of the denture in situ so the tissue can heal and an accurate impression of the untraumatized fitting surface can be taken prior to making a new, better-fitting denture.

Requirements of denture base polymers:

  • Physical properties: good esthetic, thermal conductivity, dimensional stability,“light“, radiopaque.
  • Mechanical properties: high value of modulus of elastisity,sufficient flexural strength,sufficient abrasion resistance.
  • Chemical properties: materials should be chemically inert, insoluble in oral fluids, should not absorb water.
  • Biological properties: should not be harmful to the technician, doctors and patients;should be non- toxic and non- irritant to the patients, should not be able to sustain the growth  of bacteria or fungi.

Heat-cured acrylic

It consists of powder and liquid.The major component of powder is  polymer (beads of polymethylmethacrylate), pigments(pink pigment-cadmium salts) and initiator-benzoyl peroxide ~0.5%.The liquid: monomer (methylmethacrylate), cross- linking agent(improves the physical properties of the set material), inhibitor(prolongs the shelf life of the liquid components).The inhibitor, which is usually hydroquinone, works by reacting with radicals formed within the liquid to form stabilized radicals which are not capable of initiating polymerization.The ratio of powder to liquid is  important since it controls the workability of the mix as well as the dimensional change on setting.A powder/liquid ratio by weight is 2.5:1.The mixture should be lefted for few minutes, and the mixing vessel should be closed to prevent evaporation of monomer.There are few stages of this material: „sandy“ consistency, after the short period of  time it becomes „sticky“,which forms strings of material.The „dough“ stage.The material can be moulded like plasticine and does not stick to the mixing vessel.The material is packed in the mould at this stage.Later can be „rubber“ and  „hard“ stages.
The dough is packed into a two-part gypsum mould.The excess of dough is removed, then the flask is closed again using the  pressure and the heat.The polymerization reaction itself is exothermic, so if the rate of reaction is too high, it cal lead to porosity.Under the pressure the dough flows into every part of mould and you can avoid of porosity.There are few kinds of porosity: granular porosity-it can be then there is insufficient amount of monomer to bind all the polymer beads together,evaporation of monomer.Contraction porosity-the use of insufficient dough to create an excess in the mould or the application of insufficient pressure during curing can lead to this kind of porosity.Gaseous porosity-it can be then the  temperature of dough during polymerization is rised significantly above 100.3˚C, the monomer at this temperature will boil and will produce spherical voids.

High- impact acrylic

High-impact acrylic denture base is also made by the hear- cured dough method.Impact resistance arises from the incorporation of a rubber phase into the beads during their suspension polymerization.

Autopolymerizing denture base (cold curing resines)

The autopolymerizing denture base is chemically similar to the heat- cured denture base except that a reducing agent is added to the monomer.The reducing agent is usually a tertiary aromatic amine, although barbituric acid derivates.The reducing agent reacts with the benzoyl peroxide at room temperature to produce peroxy free radicals, which initiate the polymerization of the monomer in the denture base.Autopolymerizing materials are used for repairing and relining of dentures, because their mechanical properties are weak,  and there is high residual free- momomer content.

Injection- molded plastic

The injection- molded plastics have the advantage of consistent molecular weight, but the disadvantage of capital equipment costs, and difficulties associated with attachment of teeth to the denture base.The plastics still offered for the use as injection-molded denture base acrylic are polycarbonate and nylon.They represent very small fraction of the market, although they offer a real alternative to metal dentures for patients sensitized to conventional methacrylate or to nickel or cobalt.
The technician has little leeway when using injection-molded plastics.The mold should be dry to prevent the generation of steem during molding.Patience is required to ensure the melt has reached the right temparature and cools sufficiently after  molding.Inadequate spruing will lead to underfilled molds, as can underheating the melt;overheating the melt can cause explosions, especially when polycarbonate is injected into moist molds.
Injection moldings rely almost totally on mechanical forces to retain the teeth.Low melt temperatures will cause strong forces to be  put  on the teeth  during the injection phase and  may dislodge some molars, even from plaster  molds.Depolymerization or oxidation from overheating the melt can result in porosity, loss of strength, color changes, and increased fouling.

Light- activated materials

This material consists of a urethane dymethacrylate matrix with an acrylic copolymer and has a microfine silica filler.It is supplied in premixed sheet or rope form.A base plate is made by adapting the material to a cast and polymerizing in a light chamber at 400 to 500nm(blue light).Teeth are added to the base with additional material followed by a second light exposure.The system eliminates the need for flasks, wax, boil-out tanks, packing presses, and heat processing units required for the construction of the conventional dentures.Light- activated materials contain no methylmetacrylate monomer, they may be considered for use in those patients who have demonstrated a sensitivity.polymerization shrinkage is  smaller than conventional systems.

A comparison of denture base materials

1.Heat cured         
  • good apperance
  • high glass-transition temp.
  • Easy fabrication
  • Low capital costs
  • Good surface finish

  • free monomer content or formaldehyde can cause
  • sensitation
  • low impact strength
  • fatique life too short
  • radiolucency

2.Heat cured, rubber       
  • improved impact strength
  • reinferced

  • reduced stiffness

3.Heat cured, fiber           
  • high stiffness
  • reinforced                                             
  • very high impact strength
  • good fatique life
  • polypropylene fibers make good
  • translucency
  • good surface finish
  • carbon and Kevlar fibers make
  • poor color
  • poor surface
  • easy to deflask
  • dimensional accuracy
  • capable of flexural strength than heat cured
  • no cheaper over long term
  • increased creep
  • increased free-monomer content
  • color instability
  • reduces stiffness
  • tooth adhesion failure
5.Injection molded           
  • dimensional accuracy
  • low free-monomer content
  • polycarbonate and nylon make
  • good impact strength
  • high capital costs
  • difficult mold design problems
  • less craze resistance
  • less creep resistance

6.light activated              
  • no methylmethacrylate monomer
  • decreased polymerization shinkage
  • possible improved fit compared to
  • conventional materials
  • requires little equipment
  • time savings
  • decreased elastic modulus
Denture lining materials

Permanent soft lining materials

Permanent soft lining materials are resilient polymers used to replace the fitting surface of a hard plastic denture, either because the patient cannot tolerate a hard fitting surface or to improve retention of the denture.Because the  lining is soft, its dimensional stability is important, as are its  durability and resistance to fouling.However, because by definition soft lining materials are above their glass-transition temperature when in the mouth, such physical phenomena as water absorbtion, osmotic presence of soluble components, and biodegradability play a greater role in the clinical success of a liner than  they do in the glassy polymers used as denture bases.

Acrylic soft liners

The acrylics consist of either highly plasticized intrinsically glassy polymers or soft acrylics that have a natural glass-transition temperature (softening temp.) at least 25˚C less than that  of the muoth.The plasticizer used to soften the acrylic can either be unbound to the acrylic and hence free to diffuse out during use, resulting in a loss of resilence, or it can be reacted into the cured matrix of the acrilic.

Silicone soft liners

The silicones used as soft liners can be devided into two types: room temperature vulcanizing (RTV) and heat cured.The resilence of silicones makes them at first  seem to be the ideal soft materials.However, silicones have poor tear strength, no intrinsic adhesion to acrylic denture base, and, if not properly cured, a tendency to osmotic pressure effects.RTV silicones‘ geatest drawback is their lack of adhesion, which is especially a problem around the edges of the attachment between acrylic and silicone.Heat cured silicones have in their formulation a silicone methacrylate than can polymerize into curing denture base and into the heat- cured addition silicone.The RTV silicones use a condensation cross-linking system based on organo-tin derivates such as those used in impression rubbers.Their degree of cross-linking is lower and their serviceability is low as a result, with frequent reports in the literature of swelling and buckling during use and excessive sensitivity to  denture cleansers.The rupture strength of some RTV silicones is known to deteriorate cosiderably when exposed to waterfor long periods.The heat-cured silicones achieve a greater degree of cross-linking and have much longer clinical lifetime.

Temporal soft lining materials

These materials are similar to tissue conditioners, but they are not so soft  as conditioners immediately affter setting but they retain their softness for longer, taking up to a month or two to harden.These materials are viscoelastic.Some kinds of cleansers can cause surface degradation and pitting of material.Temporal soft lining material can be used improving the fit of ill-fitting denture until such a time as a new denture will be maden.These materials will go hard, when this occurs, the surface is rough and increases the risk of trauma.In this state the base can be colonized by Candida,it leads to stimatitis.

Tissue conditioners

Tissue conditioners are soft denture lining material which may be applied to the fitting surface of a denture, to the dentures of patients who have undergo surgery.,they are useful when a tooth is being added to a denture( very shortly after extraction).The material consists of powder (polymer beads-polyethylmethacrylate) and liquid (solvent-ethyl alcohol; + plasticizer- butylphthalyl butylglycolate).

A comparison of soft liners and tissue conditioners

1. Soft liners:

a)   Acrylic      
Advantages : 
  • high peel strength to acrylic denture base
  • high rupture strength
  • some can be polished if cooled
  • reasonable resistance to damage by denture cleansers

  • poor resilience
  • loses plasticizer in time  
  • some buckle in water

b)  Silicone(RTV)   
  • resilience
  • low tear strength
  • low bond strength to dentures
  • attacked by cleaners
  • buckle in water
  • poor abrasion resistance

c)  Silicone heat cured   
  • resilience
  • adequate bond strength to acrylic
  • more esistant to aqueous environment and
  • cleanser than RTV
  • low tear strength
  • poor abrasion resistance
2. Tissue conditioners      
  • viscoelastic properties almost ideal
  • can be applied chairside
  • denture fit well
  • can record freeway space
  • low cohesive strength
  • affected by cleanser
  • alcogol can sting inflamated mucosa.

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

Cyst cannot stay at the same size. It will enlarge

(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.

  • 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.
  • 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.


  • 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.

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.
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)
Antiseptick pack

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.
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)

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. 

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
-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

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)
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.
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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Sabtu, 30 Juli 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!


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.


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