Oral Pathology lecture #6 - Web viewPulp calcification2. Periapical periodontitis3 ... systemic signs and symptoms > fever and ... Periodontal disease has shown in some studies to

Oral Pathology Lecture #6

This lecture covers three topics:

1. Pulp calcification2. Periapical periodontitis3.Diseases of the periodontium

1.Pulp calcification

Up to 20%of population may have a sort of calcification in pulp chambers and root canals which can be detected by radiographs (x-rays).Histologically; if we took histological sections, then the prevalence will be more, because part of the calcification won't appear in radiographs especially if it was small.Percentage or prevalence increases with age, also if any sort of trauma, caries occured or preexisting pulpitis , it might lead to an increase in the percentage.

Pulp calcification divided into:- pulp stones- linear calcification

Pulp stones:- calcified round masses that form within the pulp.the doctor mentions that we might find the classification different between references.- generally they're divided into true or falseit's considered true when its composition is the same as dentin (odontoblasts and dentinal tubules ..)it's considered false when it's composed of calcified tissue only.

- both can be: 1. free within the pulp chamber or root canal (far from dentin), or 2.attached to dentin(adherent) or 3.they can also be within the dentin(interstitial or embedded); they become surrounded by secondary or reactionary dentin !

- Usually they're asymptomatic, discovered by chance through radiographic examination.

- etiology is unknown, it is thought to be a result of local metabolic dysfunction inside

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the pulp or trauma then there was extravasation of cells, fibrosis, followed by mineralization and then it starts to increase in size (forms many layers).

As we mentioned before, there are different classifications, another one classifies the calcification into 1.pulp stones 2.denticles

Q.when do we call them denticles? And what is theory that explains the formation of denticles.

- Dr. here shows a radiograph of a tooth with pulp stones, in radiographs they're mostly in the coronal pulp, appear as round, small and radio opaque structures, size and number increase with age, there are also some diseases; systemic diseases or syndromes we talked about, in which there is an increase in the formation of pulp stones, one of them is Ehler Danlos syndrome, so we must know about this syndrome.

- Going back to the first classification, now we'll talk about the linear calcification, also called dystrophic calcification:Granules of calcified material scattered in large masses, and normally it's formed in the direction of blood vessels or nerves so it appears as linear distribution of small granules. Here it's mostly found in root canals more than in pulp chambers and it also increases with age.

Q.what is the clinical significance of pulp stones or calcification in general? RCT(?)

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2.Periapical periodontitis

- we say that we have caries which caused pulpitis, what happens next when necrosis occurs in the pulp? In other words, we say that bacteria entered the pulp and caused inflammation, and inflammation eventually leads to necrosis, necrosis means necrotic material, a lot of damaged cells, enzymes, bacteria, toxins and inflammatory mediators, all these will go out from the apical foramen or the lateral canals in the

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pulp and reach the periodontal ligament space and there, another process occurs which we'll talk about now that's called periapical periodontitis.

- Periapical: means around the apex, periodontitis: inflammation.

- so it's an inflammation around the apeces of teeth within the periodontal ligament.

- This area is also a confined space ( secondary to the pulp which is the most confined space), but here there is a little extent to the increase in size of the periodontal ligament space, how does this occur?

This increase in size has two directions, it can elevate the tooth and result in an increase in size, or it can cause bone resorption with time and also result in an increase in size.

Compared to pulp, 1.in periodontal ligament we have rich collateral blood supply, we know that when we have good blood supply, we have good healing and good resistance ( and this is the idea of root canal treatment, that when we do RCT and we stopped the migration of necrotic material into periodontal space, we give a chance for the periapical lesion to heal).

2. In periodontal ligament we have proprioceptive nerve fibers which detects the exact location, so if they get stimulated, patient can detect the area of pain. In the previous lecture we said that in pulpitis patient can't detect the tooth causing pain, so he comes to clinic complaining about the whole region in pain and not a specific tooth, even sometimes he can't say if it's in the upper or lower jaw! But if the inflammation reached the periapical space, there we can find fibers that locate the pain and he can say exactly what tooth is in pain, normally these nerve fibers are beneficial to let you know where you press when you eat (proprioception). So in the case of periapical inflammation it's easier to locate which tooth, and dentist can go directly to treat it, while in pulpitis he might dislocate the exact tooth and treat another one instead!Etiology: - most common cause of periapical periodontitis is pulpitis ( bacterial inflammation from the pulp)- it can be caused by a trauma to the tooth; when you're eating for example, a stone

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comes between your teeth, you pressed hard, trauma occurred in the periodontal space and inflammation resulted but in this case it's sterile and reversible.- also root canal treatment can sometimes cause it as a result of the materials used in the treatment that can get out of the apex and cause damage to the periodontal space, over instrumentation (file out of the apex) can also lead to the damage.

Nature of the inflammation (which can be acute or chronic ) depends on many factors:-- if the etiology was pulpitis, is it close or open? If it was close (pulp chamber is not open), then the pressure on the periapical region is more; all the pressure is dissipated downward! But if it was an open cavity, then the pressure is less, so less damage will result.- Bacteria (number/type/virulence/toxins produced) differs between different cases and result in different inflammations.- Immune response which is variable between individuals; good immunity results in less damage.

Periapical periodontitis can be acute or chronic.Acute inflammation can transform into acute alveolar abscess (AAA) if virulence of bacteria and damage increased.Acute inflammation can transform with time into chronic alveolar abscess if the body was able to control it.Chronic inflammation can transform into acute and vice versa.Chronic means that the inflammation took a long time around the apex and caused bone resorption and formed granulation tissue that's called periapical granuloma( associated with hypercementosis/osteosclerosis/root resorption), and this granuloma might transform into a cystic lesion that we call periapical cyst or radicular cyst.

Acute periapical periodontitis:- acute inflammation (the starting point), in which there is acute inflammatory cell infiltrate around the apex in the periodontal ligament space. Now, the accumulation of inflammatory cells, fluid and edema might cause the elevation of tooth on which any light touch may cause pain. - well localized; patient can locate which tooth.- pain not affected by temperature change, because pulp is already necrotic so it

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won't respond to temperature change.- in radiographs: because it's an acute inflammation (it has just happened), normally the periodontal space does not appear in radiographs because it contains soft tissue, but if you waited 4-5 days after the acute inflammation, you can sometimes find that the periodontal space got widened because the tooth got elevated, but you need a good radiograph to detect this minor change.- lamina dura around the apex (which is the first layer of the bony socket surrounding the periodontal ligament and root) is less clear (normally it appears whiter than the rest of the bone; it's dense bone) because inflammation can cause demineralization of this layer.- Now, if the acute inflammation was the result of trauma >> with time, it resolves (we said before it's reversible).if it was the result of an infection>> it can transform into acute alveolar abscess(pus formation) as a result of increased damage in the area and can distribute there, or it can transform into chronic periapical periodontitis where bone resorption and formation of granulation tissue occur. (all this depends on the factors we mentioned before; bacteria/immunity/open or close pulpitis ….).

Chronic periapical peridontitis (periapical granuloma):- approximately 75% of the periapical inflammation cases; so it's the most common to see.- Chronic: means inflammation took a long time around the apex and there was time for the bone to get resorbed.- in radiographs: bone resorption appears as periapical radiolucency; bone resorbed and lamina dura disappeared, and this radiolucency is continuous with the periodontal space.(in radiographs it's oval or round radiolucency with well defined outline especially if bone growth is stopped).- if you extract the tooth, you find a piece of soft tissue attached to the root(granulation tissue) which is contained in the space created in bone, actually it's not an empty space, what happened is that the bone got resorbed and the granulation tissue filled the space instead.the name periapical GRANULOMA is somehow misleading because the case here is formation of granulation tissue and not granuloma, as granuloma means a specific lesion like that created in TB (we have caseous and non-caseous granulomas), so the right thing is to call it chronic periapical periodontitis.

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Microbiology:- the bacteria present in the chronic periapical periodontitis are variable (mixed infection), most commonly present are the gram –ve anaerobes;- obligate anaerobes (prevotella spp.)- Facultative anaerobes ( strep. Milleri)

Clinically:- periapical periodontitis is usually chronic, with mild symptoms; because there is no great pressure because of bone resorption ( there is releasing of pressure), so patient might have a painless tooth or he might feel a slight tenderness on palpation.- on percussion, because normal tooth has intact underlying bone, when you hit it with the mirror handle, you will hear a high-pitched sound, but in the case of chronic periapical periodontitis which has an underlying granulation tissue, sound will certainly be different, so by doing this you can know which tooth has an underlying granulation tissue.Percussion gives 2 indications: 1-pain; means there is an underlying inflammation( needs RCT). 2- from sound you can feel what is the tissue underlying the tooth.- no response to thermal or electrical pulp testing (expected); because pulp got necrotic long time ago.

Histologically:when we take a cross-section, we can see the granulation tissue in the radiolucency, this granulation tissue consists of immature fibrous connective tissue, so you'll find fibroblasts, collagen fibers, capillaries, epithelial cells, endothelial cells of the capillaries and chronic inflammatory cells infiltrate; lymphocytes and plasma cells, you can also find acute inflammatory cells. So it's a granulation tissue that is not specific.One of the things that you can find in the periapical granuloma are the cholesterol clefts(spaces), which were originally cholesterol crystals(accumulations of cholesterol)and because of the processing in histopathological preparations they melt and spaces result in their place which are called cholesterol clefts. Where did the cholesterol come from? From the breakdown of RBCs which are extravasated outside the blood vessels, they get damaged and cholesterol gets released and accumulates in the area.

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in periapical granuloma you can also find hemosiderin deposits; granules of hemosiderin. Q.what is hemosiderin and how did it reach this area?you can also find foamy histiocytes which are macrophages, and foamy means that they have soap-like bubbles in their cytoplasm; they are distended, large macrophages with a foamy cytoplasm. Phagocytes; they engulf materials, and as a result of engulfing cholesterol and lipid materials they will acquire a foamy cytoplasm.you will also find in the periacpical granuloma foreign body multi-nucleated giant cells; thought to be a group of histiocytes that got fused together and formed one large cell with multiple nuclei the aim of which is also to engulf foreign materials like cholesterol crystals, that's why they are most apparent around cholesterol.in the periodontal ligament you will find cell rests of malassez, in normal sections they are found like strands or small islands of inactive squamous cells, if there was a periapical inflammation, they get stimulated again and start to grow and proliferate and they might form a mass of cells, and necrosis occurs in the center of this mass leading to the formation of cystic lesions inside the periapical granuloma, and these are called radicular cysts ( we'll talk about them later on ).

So, if you left the periapical granuloma without interference what happens is:- will increase in size, but will eventually stop growing.- can transform into acute alveolar abscess.- can transform into chronic alveolar abscess.(if virulence of bacteria increases acute will happen, and if the immunity rose, chronic will happen).- radicular cyst can form (cystic lesion).- in some cases instead of bone resorption, bone formation might happen, so the area around the radiolucency will appear radio dense, and this is called osteosclerosis.- periapical inflammation can lead to the resorption of the root cementum, or in some cases if it was chronic mild irritation, it can lead to hypercementosis ( clubbing of the roots ).

Acute periapical abscess:- think about the patients attending the clinics with severe, non-tolerable pain, not sleeping the night and want an immediate action from you, those patients have acute

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periapical abscesses; which means there is pus formation around the apex.- microorganisms are virulent in these patients.- usually it's associated with close pulpitis in which the pressure is greater in the periapical space.

Clinically:- patient with severe pain, distributed, uncontrolled inflammation that might result in systemic manifestations. - systemic signs and symptoms > fever and malaise.- extrusion of the tooth; patient feels an elevation in the tooth and any pressure or percussion leads to severe pain.- swelling and redness of soft tissues around the tooth, because we said that the inflammation distributed out of the area.- severe pain when percussion is performed.- doesn't respond to temperature change( it's not a spontaneous or throbbing pain; doesn't need the change in temperature).- doesn't respond to electrical stimulation because pulp is already necrotic.

Radiographically:- if it was an acute periapical inflammation and formed an acute abscess, changes might not be that detectable; just a slight widening in periodontal ligament and less clear lamina dura, the cone around it (it's a spreading inflammation) might be less dense.- if it was a periapical granuloma and transformed into acute alveolar abscess, you'll definitely detect a periapical radiolucency in the radiograph; well defined round radiolucency.

Acute alveolar abscess can transform into chronic abscess with time if you drilled into the tooth (opened the tooth), or the tooth itself opened spontaneously. The doctor shows a picture and adds that the abscess with time can open and the pressure decreases and transforms into chronic, or the patient can come to you to open an access for it to reduce the pressure and the lesion becomes chronic.so as we said, as it might transform into chronic, it also might continue as acute if left, and pus may get through 1. the root canal if the tooth was open, or 2. from the gingival sulcus through the periodontal ligament(around the tooth) or 3. it can

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distribute through the cancellous bone, reach facial spaces and cause swelling of the face.

Histopathology:

If we take a cross-section, we'll find pus, necrotic material, acute inflammatory cells, bacterial colonies, granulation tissue, and mixed bacterial infection.

As we said if left, it can reach facial spaces; buccal space, submandibular space and sublingual space and can be bilateral leading to facial swelling and severe consequences, we call this case "ludwig's angina".

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3.Diseases of the periodontium

-We're not going to get into this topic in details because there is a complete course regarding it.

- Healthy gingiva : pink, stippled, sharp appearance between teeth with interdental papillae, we have marginal and attached gingivae, no bleeding when brushing or alone and no redness or swelling.healthy gingiva is occasionally found in individuals, the most common to find is chronic gingivitis which means redness, swelling and inflammation confined to the marginal gingiva. in a picture the dr. showed > redness and swelling of the marginal gingiva and interdental papillae, this is chronic gingivitis.

- regarding chronic periodontitis, it's an inflammation or destruction that distributed beyond the marginal gingiva to the supporting structures; bone, periodontal ligament and the attachment of the gingiva to the tooth and this leads to bone loss, gingival recession or pocketing, exposure to the roots and mobility of teeth.

Risk factors (of chronic gingivitis or peridontitis):

- Like caries, which is caused by bacteria in plaque, there are specific bacteria in plaque and they're what cause the periodontal disease.

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- these bacteria are different than that causing the caries.

- the longer you leave this plaque, the higher the risk of developing a periodontal disease.

- most common bacteria are the gram negative cocci at the beginning, but if left for a longer time (individual did not brush his teeth), the thickness of the plaque will increase and it will contain further more species (gram negative/ anaerobic/motile). The idea is not to leave the plaque for long periods, as doing so will increase the risk of developing a periodontal disease (chronic gingivitis or periodontitis).

- as a conclusion, chronic gingivitis and periodontitis are plaque-induced.

But there are other risk factors(local or systemic) that can enhance the progression of the disease:

A-local factors:- alignment of your teeth; if you have good alignment, you have less risk of developing a periodontal disease, but those having crowding or problems in their teeth alignment and areas that are difficult to clean, probability of developing is higher.

- restorations; presence of restorations in general and those that are faulty or over hanged in specific may lead to collection of plaque in that area and develop a periodontal disease.

- presence of appliances; partial dentures or orthodontic appliances can increase the progression of the disease.

B-systemic factors:

- pregnancy or puberty; hormonal changes can increase the progression of the disease, pregnant ladies can sometimes have chronic gingivitis and not periodontitis, and this might be caused by the presence of the pregnancy hormone progesterone which leads to the increase in permeability of the blood vessels in the gingiva and increase in the local release of inflammatory mediators in that area which leads to the inflammation of the gingiva, we can also see an enlargement of the pregnant ladies' gingivae which we call "pregnancy epulis". اللثة تضخم

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- diabetic patients have more risk of developing a periodontal disease, the increased risk is thought to be the result of the reduced vascularity, reduced phagocytic function and immunity and increased sugar in saliva and crevicular fluid.

- Malnutrition; protein or vitamin c deficiency for example.

- Blood diseases which reduce the immunity like cyclic neutropenia; leads to more periodontitis.

- Oral contraceptive pills; leads to gingivitis in ladies.

- Corticosteroids and NSAIDS

- cyclosporine, phenytoin, Ca++ channel blockers; cause gingival hyperplasia and enlargement of the gingivae.

- AIDS patients.

- Smoking; especially in relation to the progression of the periodontal disease.

- mouth breathing (?) Q. is it related to gingivitis? And what are other complications to mouth breathing? Bone changes, gingival effects, growth of the face ….

We said that systemic diseases can affect the periodontium, but do the periodontium diseases lead to systemic diseases ?- Periodontal disease has shown in some studies to be an associated factor in coronary artery disease and in stroke!- periodontal disease in pregnancy has been associated in an increase in premature births and low birth weights.- control of diabetes in patients with periodontal disease is more difficult than those with no periodontal disease!

So some studies in the literature support the idea that periodontal diseases can lead to systemic diseases.

Chronic gingivitis: -asymptomatic, red and swollen gingiva with plaque on the gingival margins.

- etiology: ineffective teeth brushing.

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- features: brushing or minor trauma can lead to bleeding and patient feels or tastes the blood in saliva.

- for academic reasons this inflammation or gingivitis has 4 stages.

- if this inflammation was left for a long period, some patients may develop periodontitis. Not all patients with gingivitis develop periodontitis.

- the 4 stages of gingivitis are:1.initial gingivitis2. early gingivitis3.established gingivitis4.periodontitis/advanced lesion

- Initial lesion:

- subclinical.- starts 2-4 days after exposure to plaque(if individual didn't brush for 4 days, initial lesion starts) and it's not apparent clinically.- localized around the base of the gingival sulcus; changes related to the area of the gingival sulcus, these changes are: vasodilatation of capillaries, fluids and neutrophils migration to that area.- because there is fluid extravasation, crevicular fluid amount will be more than normal but it isn't that visible clinically.- attached or junctional epithelium connecting the gingiva to the tooth starts to get disrupted.

- Early lesion:

- if left more than 4 days till one week after exposure to plaque, neutophils will increase in number.- impairment in junctional epithelium increases.- acute inflammation with neutrophils strats to change into chronic, so lymphocytes start to appear instead of neutrophils.- damage to fibroblasts which synthesize collagen fibers.

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- Established gingivitis:

- here symptoms start to appear, if left more than 2-3 weeks without tooth brushing.- more damage to the junctional epithelium.- pocket or circular epithelium starts to get damaged or ulcerated, ulceration means beginning of bleeding, blood appears when brushing or when minor trauma occurs.- area becomes red in color.- inflammation involving plasma cells instead of lymohocytes, so more destruction to the gingival connective tissue.- volume increases, so swelling occurs in gingiva, sometimes repair occurs in the area because of chronic inflammation, repair leads to chronic hyperplastic gingivitis; so in some patients there's production leading to formation of granulation tissue leading to the enlargement of the gingiva which is called "chronic hyperplastic gingivitis", clinically apparent as enlargement of the gingiva in area of marginal gingiva, it's not only edematous but also fibrous.

- Advanced lesion/periodontitis:

- not all gingivitis cases progress into periodontitis.- destruction of the connective tissue attachment of the roots; damage to the gingivae attached to roots, so bone loss will result; bone resorption between teeth, junctional epithelium attachment will become lower, and the shallow sulcus becomes deep that you can insert a probe in that area, this process is called "pocket formation".- earlier evidence: - chronic inflammation from the base of junctional epithelium, inflammation goes downwards leading to resorption of the bone and damage to the connective tissue attachments, this results in what is called "apical migration of the junctional epithelium" and pocketing.

Clinically how to distinguish periodontitis:- red, swollen gingiva; like those of gingivitis.

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- gingival bleeding.- pocketing; when using a probe and measuring the depth of the sulcus, so you know if there is pocketing or not.- recession of gingiva.- loosening of teeth; see if there is mobility; it’s a sign of peridontitis because it means bone resorption.- unpleasant taste or halitosis; because there is pocketing which leads to bacterial accumulation, bad breath and an unpleasant taste.

Radiographically:

- at the beginning, bone between teeth, instead of being triangular, it becomes blunt (blunting of the alveolar crests is an early changing).- later one there is horizontal bone loss and super bony pockets; all bone becomes uniformly resorbed, and this is called "horizontal bone loss".bone was reaching cementoenamel junction, now it all got resorbed, radiographs help in diagnosing periodontitis.- in some cases, in some teeth you don't have horizontal bone loss but instead "vertical bone loss"!

Factors related to increase in the vertical bone loss:- malalignment.- restorations between teeth; class 2 overhang.- occlusal trauma.All these can lead to more vertical bone loss.

Good Luck!

Ameer A. Frangieh

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Oral Pathology lecture #6 - Web viewPulp calcification2. Periapical periodontitis3 ... systemic signs and symptoms > fever and ... Periodontal disease has shown in some studies to