INFLAMMATORY JAW LESIONS

2009-12-11

15 people showed up to this lecture. Good for you if youre one of them. The two pictures above are what were written on the board at the beginning of lecture. INTRODUCTION There are not a lot of inflammatory jaw lesions (its actually the shortest chapter in the book). Inflammatory jaw lesions are the bread and butter of endodontics, probably half of oral surgery, and a significant amount of dentistry. Dr. Levy goes over some traumas to a tooth: Bacteria can go through a tooth and lead to its destruction via dental caries We can physically traumatized a tooth (ex. a fall, a punch) o A dentist can cause trauma (ex. drills into healthy tooth, heat pulp while drilling) It doesnt matter what the trauma is, the body only has one reaction to physical assault: inflammation. What are the cardinal signs of inflammation? redness, heat, swelling. If you were to hit a tooth with a hammer, you would cause redness in the pulp. Blood vessels would dilate and inflammation would occur. Can the pulp swell? It aint got nowhere to go. The pulps trapped inside the tooth. PULPITIS If you cause damage of any sort (ie. electrical damage, cold damage, heat damage, physical damage, bacterial assault, etc.), whats going to happen is the pulp develops pulpitis, which is inflammation of the pulp. There is nowhere for the pulp to swell, so pain will occur because of the pressure on nerves inside the pulp. Because the only opening of a tooth is at the bottom, the pulp tissue will want to swell towards the apex of the tooth. This will cause pressure on the blood vessels that feed the pulp at the apex and block the blood supply to the pulp. He uses the concept of a tourniquet to explain what would happen. If you were bleeding from the arm, you would wrap a tourniquet around it to cut off the blood

supply and stop it from bleeding. If you left this tourniquet on for a couple of days, youre arm would die. The same thing that occurs in the arm with a tourniquet happens in the tooth during pulpitis. When the pulp swells, it closes off the blood vessels of the pulp. This deprives the entire pulp of a blood supply and the pulp dies. When the pulp dies, it is known as pulpal necrosis. PERIAPICAL ABSCESS In the situation of the dead arm, you would have to amputate the arm, because the dead tissue will cause damage to live tissue. The products of death and necrosis and necrotic tissue will harm living tissue. If pulpal necrosis occurs, and the necrotic tissue of the pulp gets into the bone, this will cause a periapical abscess. An abscess can resolve in two ways: 1. Draining abscess He points to the mesial root (which is the root on the right in the picture on the top left) and says that a hypothetical abscess is at the red dot at the apex of that root. In this particular example, the abscess is caused by caries, which means that its not only an abscess, but its a septic abscess because it has bacteria in it. This abscess at the end of the root is going to have pus. By definition, when we say there is an abscess, we say theres pus. Pus is dead neutrophils, and in this case bacteria. So that (I believe when he says that, he is referring to pus or necrotic pulp) is going to spread through the tissue gradually, and if it finds a way out, then itll drain out of the skin or in the mouth. That will become a draining abscess and the pathway is called a sinus tract. One of the most common mistakes he sees with dentists that send him biopsies is that theyll say a sinus track. It is NOT a track. Its a tract and that means something running through tissue. If an abscess drains, what will happen to the pain? The pain will go away because the pressure is gone. So if the pus finds a way out, the patient will know it right away. Most of these abscesses drain in the mouth and the patient can detect it by having a bad taste in their mouth. Clinical symptoms of an abscess that drains into the mouth: Tooth ache (pain) goes away. You can tap the tooth with your mirror (percussion test) and it wont hurt because the pressure is gone. Bad taste in the mouth after tooth ache. If the abscess drains into the skin, then the patients can have an ugly looking draining yuck on their face. 2. Periapical cysts On the other hand, sometimes the periapical abscess stays at the apex of the root for a long time. It enlarges a bit, but the body (if a patient is pretty healthy) will try to fight it. When the body fights an

insult, we get chronic inflammation (he doesnt say it but I assume he means over a period of time, though we learned there are times when inflammation goes straight to chronic so I dunno), and we will now have granulation tissue forming around the abscess and this is what a periapical granuloma is. It is the body trying to fight off what was an abscess. In some patients, eventually the whole abscess subsides and the whole thing becomes a granuloma and there is nothing else there. Granulomas CAN hurt if there is pressure put on them, so if you tap the tooth, sometimes they hurt because they are expansile and theyre in the bone. But granulomas hurt less than the abscess because the abscess is acute inflammation. Now, lets say the patient had caries or trauma, the tooth died, lesion from the periapical lesion was an abscess and its now become a granuloma and lets say this granuloma stays there for a long time because the patient doesnt want to go to a dentist and hes become used to the pain. In this area [he points to the area where the periapical granuloma is (the root on the left in the picture on the top left)], there are a lot of rests of malassez, which are epithelial debris from when teeth form that are found in the periodontal ligament tissue. Sometimes, these rests like to grow. If these rests grow in the granuloma, it will form an epithelial lining between the bone and the granuloma. This epithelial lined granuloma is known as a periapical (or radicular) cyst. Cysts come from granulomas. You must have had at some point in time a chronic inflammatory response before the cyst can happen. Hypothetical situation: Lets say a patient has a periapical cyst due to caries and he does nothing about it. One day this patient eats some stuff that has fairly active bacteria in it and this bacteria gets shoved down through the caries lesion into the pulp. The patient then chews gum that causes constant pressure on the pulp and pushes the bacteria down even further towards the cyst. That cyst can get reinfected. If that cyst gets reinfected and acute inflammation occurs, the cyst can break down and form an abscess. That abscess can then become more chronic and long standing, it can become a granuloma, and if there is still epithelium around it can regrow and become a cyst again. So these things can change biologically. If he gets a biopsy and he sees evidence of a cyst that is degenerating and starting to break down and form an abscess, he will just call it a cyst with acute inflammation and he wont explain what it really is because he doesnt want to confuse the dentist or endo who sent it to him. For the dentists who send him biopsies, everything is nice and simple. They send him a periapical lesion, and he gives them back one of the three diagnoses: abscess, granuloma, or cyst. The reality is it is not unusual to have a mixture where sometimes all three stages are visible in the microscope. These things are dynamic and they can change and be altered, but for purposes of diagnosis the microscope can tell you which it is. Question from class I cant hear. Answer: Sometimes the cyst gets so big that it breaks through the wall of the bone and then it drains itself out. ACUTE OSTEOMYELITIS Hypothetical situation: You have 69 or 70 year old patient in semi-good health, theyre kind of a little run down: maybe they have a heart disease or a lung disease, and they develop a periapical abscess. This patient may not have the tissue oomph to generate granulation tissue and make the whole thing go chronic. The sinus tract may not form either. It may well be that the abscess just starts to spread into the bone. If this occurs, this is known as acute osteomyelitis.

Acute osteomyelitis is very painful. In the old days before antibiotics, a kid may fall and damage a long bone in the leg and get an infection in that damaged bone. Acute osteomyelitis of a long bone could then develop from that infection and the kid may end up losing the leg because of it. In the mouth, what can happen is acute osteomyelitis can spread to adjacent teeth, and you would end up with a patient with 4 or 5 loose teeth sitting in bone thats being destroyed with pus. What you would have to do is take out a bunch of teeth, load the patient with antibiotics, and maybe even give them hyperbaric oxygen in order to overcome this large infection. CHRONIC OSTEOMYELITIS If a patient has an acute osteomyeltis and they respond to antibiotics, then it will develop into chronic osteomyelitis. Chronic osteomyelitis is not rare and we see it periodically. Assuming the antibiotics were started when the acute just began, you may not lose a bunch of teeth and you may not lose a lot of jaw. A lot depends on how quickly the acute osteomyelitis is brought into the chronic stage. There are different types of chronic osteomyelitis: Chronic Proliferative Parostitis (Garres osteomyelitis) : This type of osteomyelitis is common in children. It is a scary lesion because radiographically it looks exactly like a Ewings Sarcoma. What happens is that they have an acute osteomyelitis that becomes chronic, but some of the bacteria that caused it leaks through the cortical bone and separates the periosteum from the cortical bone, just like an Ewings sarcoma would. Whenever you move periosteum from cortical bone, periosteum makes new bone and what happens is you get the onionskin appearance. You get multiple layers of cortical bone and it looks like an onion youre slicing in half on an x-ray. This type of osteomyelitis is treated with antibiotics. It occurs mainly in young people (pre-teens and teens) and males more than females. It may present with more swelling than pain and discomfort. It starts as an acute osteomyelitis, but it becomes chronic quickly (probably because the pre-teen/teen is pretty healthy and they have a lot of tissue ability to adapt) even if they dont get antibiotics and you will see a big swelling. It is much more common in the mandible than the maxilla. Chronic Diffuse Sclerosing Osteomyeltis: A typical patient who may develop this is going to be in their 50s or 60s with lots of carious lesions, lots of periodontal disease, poor dental health, but pretty good physical health. Radiographically, you will see large blobs of opaque material in the mandible, and sometimes in the maxilla, around the apices of the teeth. It wont look like a cementoma type thing. It will be multiple snowballs in the jaws. These patients are difficult to treat because what happens is that a great deal of their bone marrow is being replaced with very dense bone from chronic inflammation, which compromises the blood supply to the bone. This dense bone makes extractions difficult, and even if the extraction is successful, the tissue may not heal well because there is not a lot of bone marrow and blood supply remaining in the bone and an acute osteomyelitis may develop as a result. If you choose to treat chronic diffuse sclerosing osteomyelitis with extractions, you should place the patient on antibiotics before and after surgery and you should try to do as little fancy surgery as possible with the extraction. He says this is not a good subject for flaps and osteoplasty and all this other stuff. The other method of treatment, which he recommends highly, is to refer this patient to an oral surgeon whom you do not know. You dont want to send this patient to a friend because you may lose that friend due to the frequent problems these patients encounter with extractions. Hyperbaric oxygen works for these patients, but its expensive.

Question I cant hear from class. Answer: Yeah, then youre going to put them on antibiotics, they may need hyperbaric oxygen Another question I cant hear. Answer: Oh yeah, thats the reason why I think this subject is worth a lecture and not just reading the book because what were dealing with is a whole bunch of interrelated dynamic things. These arent snapshots, ok? I can give you snapshots of each one of these, and I do, but the reality is in the human being, these things can go back and forth. Garres does not. Garres comes from chronic osteomyelitis and stays Garres until its cured. But all this other stuff can zigzag back and forth, which makes life complicated. Its not so easy to treat. Back to chronic diffuse sclerosing osteomyelitis. This is not a common disease in well to do suburbs, but hes seen it the most here because we have a huge patient population that are aged and have poor oral hygiene, bad teeth, lots of periodontal disease, and lots of caries. Focal Sclerosing Osteitis (Condensing Osteitis): If you have a patient, and you see a small radiopacity somewhere in the jaw and you show it to Dr. Levy, hell tell you its a focal sclerosing osteitis. If you show it to an old clinical dentist, theyll tell you its a condensing osteitis. Condensing osteitis is a term that was used in the 40s and 50s. A focal sclerosing osteitis is an area of dense bone, usually from a previous infection. This dense bone remains for the rest of a patients life. It is asymptomatic (does NOT cause pain) and requires no treatment. It can be located anywhere where there was a previous deciduous tooth; it can be anywhere where there was a chronic infection (ex. a patient may have had chronic periodontal disease that was very focal in one little area of the jaw and they end up with dense bone in that area).