Pedo
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Developmental dental anomalies Dr.said: 1-Most of the questions that you get in your final exam "spot exam" are on photos like that shown in the lecture. 2-she will not give us the slides and you can study this lecture from the book chapter7 in Cameron & Widmer. 3-always remember the developmental stages of a tooth formation, where you get induction, proliferation, histodifferentiation, morphodifferentiation, matrix deposition, and finally mineralization. 4-you have to remember all the eruption dates, development dates, root formation dates and the calcification dates; the table that I told you about. There will be questions about it in the exam.
1-hypodontia : The loss of small number of teeth (less than 6 teeth)
&
oligodontia
&
The loss of large number of teeth (more than 6 teeth)
anodontia
NO teeth at all
The incidence of hypodontia is 0.1-0.7% in primary dentition and 29% in permanent one. The incidence is 3rd molar, then maxillary lateral incisor, then the 2nd premolar then mandibulr central incisor.
If you don't have your 52(it was congenitally missing) will you have your 12? It will be missing too, BUT why?????? Because it's a successor and it forms from the dental lamina of 52 so this (52) is not there then 12 will be congenitally missing. So if you have one deciduous tooth missing so the permanent successor will also be missing, but the opposite is not true(in some cases you have the primary tooth there but the permanent one is not there).
The syndromes which are associated with hypodontia: Ectodermal dysplasia: It's a group of conditions which affect the Ectodermal germ layer when the embryo is growing. So skin, nails, hair and the enamel (the only tissue of the tooth develop from the ectoderm), and other Ectodermal tissue in origin will be affected. Cleft lip and palate: is a condition associate with many dental abnormalities such as hypodontia, supernumerary teeth, dilacerations, etc… Craniosynostosis: a defect in the bony structure of the face it's not just a lip or a palate. Trisomy 21 "Down syndrome " Chondroectodermal dysplasia: type of Ectodermal dysplasia. Oral facial digital syndrome. The treatment aims: Reduce pain Get masticatory function, speech, esthetic and vertical dimension.
Girl with Ectodermal dysplasia: Photograph: 1-her hair looks normal but if you see it (hair) under the scanning electron microscope you will see the proteins are defective. You have to know that there are degrees of the disease because it's caused by multiple genes so the phenotype will be different from one to another, so in some cases there will be no hair at all and in other the hair is not really affected as much as the saliva. 2-the ears are pointed and triangular. 3-the face is more like a triangle 4- Class III malocclusion because most of them have hypoplasia of the maxilla so the mandible will grow a little bit further. Opg: 1-agensis of 52 and 62 and of course no successors 12 or 22 underneath them. The best thing is to look an OPG always count from the midline to the end, each quadrant separately.
Are we supposed to see them at this age (she's 6.5 years)? Yes Are we supposed to see 7s right now? Of course you should, you are supposed to see the 7s at age 2.5 years old; you can see the bud at this age.
9 years old girl: It was her first visit to the dentist when she lost her 71, 81 with no teeth replaced them, so we took a radiograph for her and found that her 31, 41 were congenitally missing. But if she went to the dentist at earlier age this will not be an issue and could be managed earlier.
Another girl: She had craniosynostosis which affects the whole face; also she had cleft lip and palate Intraorally: 1-She had a problem in the central incisor which was rotated and when it was erupted its edge was sharp so it caused injure to the lip resulted in a gross ulcer, it was very painful to the patient. 2- She had some deciduous teeth were retained and carious. Treatment: 1-Dr.ola extracted the deciduous teeth. 2-she did a sectional fixed appliance to her to derotate the central incisor 3-she left a primary tooth because there is a bony defect so it will preserve the alveolar bone. 4-she also left the lateral incisor but because the central was rotated so it was hard to remove it because there was no access to it, until she derotate the central and then she extracted the lateral.
Another case: This is Down syndrome you can see the features: 1- Small ears. 2- oblique eye Fissures. 3- Protruding tongue.
2-supernumerary teeth: Terms used for supernumerary teeth: According to the site: **mesiodens: it's a tooth that erupt between the two centrals in the midline, but sometimes this mesiodens will block the path of
eruption of one central so you will not see the typical picture (two centrals and a mesiodens between them). **paramolar: it's parallel to the molar and buccally placed. **distomolar: it's distal to the molar. According to the shape: **conical **tuberculate (am not sure): had multiple cusps **supplemental: which looks exactly the same as the one next to it. **inverted conical: it's a conical one but erupted in an opposite direction, some of them can even erupt into the floor of the nose or into the maxillary sinus. The incidence of supernumerary teeth is 0.3-0.8% in primary dentition and 1-3.5% in permanent one. 98% of the cases occur in the maxilla. 75% of the cases are mesiodens (commonest type). The syndromes which are associated with supernumerary teeth: Cleidocranial dysplasia: Its features are: 1-Cleido: refers to the clavicle, it's either short or absent so the shoulder will be brought forward easily. 2-Cranial: the bones of the cranium will be flat. 3-cranial synostosis: the fontanels haven't closed yet. 4-we have supernumerary teeth and thin cementum. Odontomes: Complex Odontome: is a developmental tumour-like mass consisting of disorderly arranged dental tissue. Compound Odontome: is a developmental tumour-like mass consisting of numerous small discrete, tooth-like structures called denticles. Dentigerous cyst.
This patient came to the clinic because his tooth hadn't erupted yet, because the supernumerary tooth was blocking its path of eruption. So I extract the supernumerary tooth and then that tooth erupt right away but if it was late we properly need to expose the crown by make an incision in the gingiva.
3-macrodontia: It's a big tooth, but why someone will end up with macrodontia? Student answered: fusion and gemination.
Dr.said: they are not macrodontia they are a defect in tooth shape and number, we have: 1-Generalized macrodontia: where all the teeth are big and that's mostly genetic or due to a systemic condition. 2-localized macrodontia: where we have one tooth is so big BUT how is that happened? Because it has a lot of blood supply because of haemangioma or tumor of blood vessels is next to it (commonest reason). ** Localized macrodontia is more common than generalized one. The treatment: 1We try to section it with the bur to make it smaller and then do a composite resin. 2We make a composite build up of the one next to it; to make them similar. 3You can extract it and do a removable partial denture.
This patient attended to the clinic because he had no space for the canine to erupt because of macrodontic tooth and in another site of the jaw there was a lot of space. Treatment: 1-we did space analysis. 2-we were planning to do orthodontic treatment so we took lateral cephalograph and on it we found that he had calcification in cervical lymph node which we concerned about (because in these anomalies they could be associated with syndromes or other problems so you must NOT ignore these patients it might be nothing but you should follow your patient) so we took CT scan and refer him to a radiologist but it was nothing, it was just because of long standing infection "tonsillitis". 3-we found out that he didn't have enough space for canine to erupt so we have to remove the macrodontic tooth in order for the canine to erupt. 4-then if the space doesn't close so we manage that either by composite resin or implant. Clinically: We extracted the tooth and then we placed removable appliance "space maintainer" in order for the canine to erupt.
4-microdontia: It's a small tooth. It can be: 1-true: all the teeth are microdontic but this is rare. It can be hormonal or genetic; also it could be relative to the jaws. 2- Localized.
An example of that is peg shape ( )على ذمة اسيل بشبه سيخ الشاورماlateral incisor which is very common. You can manage them by composite resin or strip crowns orthodontic to close the spaces or you can extract them and construct a partial denture or implants.
This is a peg shape lateral incisor and this is familial, that's mean the father had it then one of his children or more will have it. It's affected by minimal pentrance polygonal genes they don't reach the whole family and they have variable expressionso the father might have the right lateral incisor as a peg shape while the son has it on the left side and it may be bigger than his father.
This patient has deciduous teeth, lateral incisor is congenitally missing and the other teeth are microdontic. So we closed the spaces for her and then we did strip crowns build up because she didn't want anything invasive like implant, extraction or partial denture.
5-Fusion and gemination: Dr said sometimes it's hard to tell either is it fusion or gemination so the best thing is to call them conjoined teeth.
This patient has conjoined teeth we took an x-ray, and we found out that the pulps of the teeth are communicating but in some cases each tooth has its own pulp so you can section them then place some composite resin.
6- Dens invaginatus& dens evaginatus. 7- Talon cusp: It's an extra cusp presents on the incisor tooth on the palatal aspect, so it's actually a pointed cusp which will interfere with the occlusion of the patient so what we do? We reduce it gradually, we remove 1 mm and let the pulp heals and the secondary dentin forms and after 2 months we remove another 1 mm and so on. BUT why we don't remove it at one time? Because it contains pulp tissue so we will expose the pulp.
8-taurodontism: It's enlargement of pulp chamber at the expense of the root. (وعلى )قولة الخصيب خصر ساحل The syndromes which are associated with taurodontism: Ectodermal dysplasia: Tricho-dento-osseous syndrome.
Klinefelter syndrome. Amelogenesis imperfecta.
What's hard about this? If this tooth get infected and you want to do RCT it's a BIG problem because the bur have to go deeper than the level of the bone in order to gain access. So if you find this early enough on an OPG, seal the fissure of that tooth and protect it as much as possible and worn the patient if any thing goes wrong with that tooth properly it will not be manageable and thus they will go to a specialist who's very expensive. **some times the pulp tissue enlarged at the expense of dentine & enamel, and that occurs especially in cases which involve the dentin in the pulp, you can call them cousin ( )زي ولد العمanything goes wrong with the dentin the same thing will affect the pulp, like these cases which affect both of them: • Vitamin D resistant rickets (VDRR). • Vitamin D dependant rickets (VDDR). • Hypophosphatasia • Dentinogenesis imperfecta. • In some cases regional odontodysplasia. These teeth are very fragile it's very easily for microorganism to cause caries and then inflamed the pulp even a simple wear will cause pulpal inflammation and abscess, so that's why you will hear about spontaneous abscess in these patients.
9-enamel chronological defect: Ola said"
"here I'll write exactly what dr.
This is due to environmental causes. **could be quantitative (hypoplasia) or qualitative (hypomineralization). **clinically: manifest as discoloration opacities & enamel hypoplasia. **could be localized or generalized. **Extrinsic staining: It's caused by chromogenic bacteria which produce byproduct causing discoloration to the tooth. You can see black staining, orange, and red one, these can be removed by tooth brushing, prophylaxis or by scaling. **Enamel hypoplasia **Cheese molars like in MIH they look like cheese. **Enamel hypomineralization and opacities.
**Amelogenesis imperfecta. **Dentinogenesis imperfecta: the color of dentin in this condition is grayish or bluish. In most cases of dentinogenesis imperfecta the pulp gets constricted and calcified **Dentine dysplasia: 1-radicular type: the dentine of the root portion is affected, it's short and thin. 2- Coronal type: It affects the coronal portion. **VDRR: rickets is a type of vitamin D deficiency. So it's a defect in mineralization (because there is a defect in calcium & phosphate) the matrix of the bone "ostoid" deposited but it wasn't mineralized. VDRR: genetic type of rickets It's X-linked familial hypophosphataemia rickets. ** X-linked: the gene that causes this rickets is carried on the X chromosome. ** Familial: it exists in families. ** Hypophosphataemia: decrease in blood P, even if you give the patient supplement.
BUT WHY? Because this genetic disease affect the kidney causing a failure of the distal tube in reabsorption of P so all the P will be eliminated in he urine. **so the p will have hyperphosphaturia & hypophosphataemia. Why there is a defect in calcium & phosphate? There are many causes for rickets: Vitamin D deficiency which is important for absorption of Ca & P from GIT. Absorption problem in the intestine which will not absorb nutrients. Or any thing wrong with the cycle which Vitamin D goes through. Malfunctioning kidney because it's very important for both of them, if the level of Ca & P is high it will get rid of this high amount but if they are less than normal it will reabsorb every molecule back to blood stream The hormones that control Ca & P like parathyroid and calcitonin hormones, so any problem in these hormones will affect them. The enzymes that control Ca & P like alkaline phosphate (important for build up bone) and acidic phosphate (important for bone resorption).
10-preeruptive intracoronal resorption of dentine (peird): -it is rare 0.6% in population. It's interesting because it looks like caries but it happens before the tooth eruption so you look at the tooth bud on an OPG inside the bone and you can see dentine resorption. There are many theories that explain this, but the most accepted one said: "osteoclast from the bone enter through some sort of leak in the enamel then they go inside and start resorping the dentine and later on you will find macrophages and inflammatory cells and when the tooth erupted the cavity will be hybrid with microorganisms" You can't diagnose this unless you have a pre-eruptive OPG because it appears as caries, even if you took a biopsy from the cavity and send it to the lab they will tell you that this is caries because the cavity will be hybrid with microorganisms. Or you can diagnose them by asking about the time "how long has the tooth been in the mouth?" So what is your differential diagnosis when you see such a tooth? 1- Caries. 2- PEIRD. 3- MIH in very sever cases; the tooth erupted very weak so enamel could break down very soon after its eruption. SO unless you have a pre-eruptive OPG you can doubt it but you can't be sure. Treatment: 1-after it erupts; you can remove it just like any carious lesion and place a filling. 2-in some cases where these cases were discovered early, they do a flap, remove bone, and fill the tooth with GI until it erupts, and then they do a proper restoration.
9 years old patient, she complained from pain of this 36 it looks normal so we took a radiograph. There was radiolucent inside the crown and around the root apex, she had an abscess and that what causes pain for her. Dr said: "this was the only case that even though I didn't have a pre-eruptive OPG I was so sure that this is PEIRD because there was no sign of caries"
11-eruption problems: Dr said: "you have to study them from 3rd year lecture"
1Eruption hematoma. 2Ankylosis of teeth. 3Erosion: is loss of tooth structure through chemicals It's important for you to know about gastro-esophageal reflex disease: the acid of the stomach become regurgitated into the throat very often during the day. It happens in young children and don't realize it as something wrong because they don't complain, so if you have a look to their mouth you will see the entire palatal surface undergo erosion. You see in pedo clinic that many patients have tooth wear, part of it is caused by attrition. Recent studies say that attrition can't happen without erosion, so erosion is very essential component of attrition.
Done
by:
1-hypodontia : The loss of small number of teeth (less than 6 teeth)
&
oligodontia
&
The loss of large number of teeth (more than 6 teeth)
anodontia
NO teeth at all
The incidence of hypodontia is 0.1-0.7% in primary dentition and 29% in permanent one. The incidence is 3rd molar, then maxillary lateral incisor, then the 2nd premolar then mandibulr central incisor.
If you don't have your 52(it was congenitally missing) will you have your 12? It will be missing too, BUT why?????? Because it's a successor and it forms from the dental lamina of 52 so this (52) is not there then 12 will be congenitally missing. So if you have one deciduous tooth missing so the permanent successor will also be missing, but the opposite is not true(in some cases you have the primary tooth there but the permanent one is not there).
The syndromes which are associated with hypodontia: Ectodermal dysplasia: It's a group of conditions which affect the Ectodermal germ layer when the embryo is growing. So skin, nails, hair and the enamel (the only tissue of the tooth develop from the ectoderm), and other Ectodermal tissue in origin will be affected. Cleft lip and palate: is a condition associate with many dental abnormalities such as hypodontia, supernumerary teeth, dilacerations, etc… Craniosynostosis: a defect in the bony structure of the face it's not just a lip or a palate. Trisomy 21 "Down syndrome " Chondroectodermal dysplasia: type of Ectodermal dysplasia. Oral facial digital syndrome. The treatment aims: Reduce pain Get masticatory function, speech, esthetic and vertical dimension.
Girl with Ectodermal dysplasia: Photograph: 1-her hair looks normal but if you see it (hair) under the scanning electron microscope you will see the proteins are defective. You have to know that there are degrees of the disease because it's caused by multiple genes so the phenotype will be different from one to another, so in some cases there will be no hair at all and in other the hair is not really affected as much as the saliva. 2-the ears are pointed and triangular. 3-the face is more like a triangle 4- Class III malocclusion because most of them have hypoplasia of the maxilla so the mandible will grow a little bit further. Opg: 1-agensis of 52 and 62 and of course no successors 12 or 22 underneath them. The best thing is to look an OPG always count from the midline to the end, each quadrant separately.
Are we supposed to see them at this age (she's 6.5 years)? Yes Are we supposed to see 7s right now? Of course you should, you are supposed to see the 7s at age 2.5 years old; you can see the bud at this age.
9 years old girl: It was her first visit to the dentist when she lost her 71, 81 with no teeth replaced them, so we took a radiograph for her and found that her 31, 41 were congenitally missing. But if she went to the dentist at earlier age this will not be an issue and could be managed earlier.
Another girl: She had craniosynostosis which affects the whole face; also she had cleft lip and palate Intraorally: 1-She had a problem in the central incisor which was rotated and when it was erupted its edge was sharp so it caused injure to the lip resulted in a gross ulcer, it was very painful to the patient. 2- She had some deciduous teeth were retained and carious. Treatment: 1-Dr.ola extracted the deciduous teeth. 2-she did a sectional fixed appliance to her to derotate the central incisor 3-she left a primary tooth because there is a bony defect so it will preserve the alveolar bone. 4-she also left the lateral incisor but because the central was rotated so it was hard to remove it because there was no access to it, until she derotate the central and then she extracted the lateral.
Another case: This is Down syndrome you can see the features: 1- Small ears. 2- oblique eye Fissures. 3- Protruding tongue.
2-supernumerary teeth: Terms used for supernumerary teeth: According to the site: **mesiodens: it's a tooth that erupt between the two centrals in the midline, but sometimes this mesiodens will block the path of
eruption of one central so you will not see the typical picture (two centrals and a mesiodens between them). **paramolar: it's parallel to the molar and buccally placed. **distomolar: it's distal to the molar. According to the shape: **conical **tuberculate (am not sure): had multiple cusps **supplemental: which looks exactly the same as the one next to it. **inverted conical: it's a conical one but erupted in an opposite direction, some of them can even erupt into the floor of the nose or into the maxillary sinus. The incidence of supernumerary teeth is 0.3-0.8% in primary dentition and 1-3.5% in permanent one. 98% of the cases occur in the maxilla. 75% of the cases are mesiodens (commonest type). The syndromes which are associated with supernumerary teeth: Cleidocranial dysplasia: Its features are: 1-Cleido: refers to the clavicle, it's either short or absent so the shoulder will be brought forward easily. 2-Cranial: the bones of the cranium will be flat. 3-cranial synostosis: the fontanels haven't closed yet. 4-we have supernumerary teeth and thin cementum. Odontomes: Complex Odontome: is a developmental tumour-like mass consisting of disorderly arranged dental tissue. Compound Odontome: is a developmental tumour-like mass consisting of numerous small discrete, tooth-like structures called denticles. Dentigerous cyst.
This patient came to the clinic because his tooth hadn't erupted yet, because the supernumerary tooth was blocking its path of eruption. So I extract the supernumerary tooth and then that tooth erupt right away but if it was late we properly need to expose the crown by make an incision in the gingiva.
3-macrodontia: It's a big tooth, but why someone will end up with macrodontia? Student answered: fusion and gemination.
Dr.said: they are not macrodontia they are a defect in tooth shape and number, we have: 1-Generalized macrodontia: where all the teeth are big and that's mostly genetic or due to a systemic condition. 2-localized macrodontia: where we have one tooth is so big BUT how is that happened? Because it has a lot of blood supply because of haemangioma or tumor of blood vessels is next to it (commonest reason). ** Localized macrodontia is more common than generalized one. The treatment: 1We try to section it with the bur to make it smaller and then do a composite resin. 2We make a composite build up of the one next to it; to make them similar. 3You can extract it and do a removable partial denture.
This patient attended to the clinic because he had no space for the canine to erupt because of macrodontic tooth and in another site of the jaw there was a lot of space. Treatment: 1-we did space analysis. 2-we were planning to do orthodontic treatment so we took lateral cephalograph and on it we found that he had calcification in cervical lymph node which we concerned about (because in these anomalies they could be associated with syndromes or other problems so you must NOT ignore these patients it might be nothing but you should follow your patient) so we took CT scan and refer him to a radiologist but it was nothing, it was just because of long standing infection "tonsillitis". 3-we found out that he didn't have enough space for canine to erupt so we have to remove the macrodontic tooth in order for the canine to erupt. 4-then if the space doesn't close so we manage that either by composite resin or implant. Clinically: We extracted the tooth and then we placed removable appliance "space maintainer" in order for the canine to erupt.
4-microdontia: It's a small tooth. It can be: 1-true: all the teeth are microdontic but this is rare. It can be hormonal or genetic; also it could be relative to the jaws. 2- Localized.
An example of that is peg shape ( )على ذمة اسيل بشبه سيخ الشاورماlateral incisor which is very common. You can manage them by composite resin or strip crowns orthodontic to close the spaces or you can extract them and construct a partial denture or implants.
This is a peg shape lateral incisor and this is familial, that's mean the father had it then one of his children or more will have it. It's affected by minimal pentrance polygonal genes they don't reach the whole family and they have variable expressionso the father might have the right lateral incisor as a peg shape while the son has it on the left side and it may be bigger than his father.
This patient has deciduous teeth, lateral incisor is congenitally missing and the other teeth are microdontic. So we closed the spaces for her and then we did strip crowns build up because she didn't want anything invasive like implant, extraction or partial denture.
5-Fusion and gemination: Dr said sometimes it's hard to tell either is it fusion or gemination so the best thing is to call them conjoined teeth.
This patient has conjoined teeth we took an x-ray, and we found out that the pulps of the teeth are communicating but in some cases each tooth has its own pulp so you can section them then place some composite resin.
6- Dens invaginatus& dens evaginatus. 7- Talon cusp: It's an extra cusp presents on the incisor tooth on the palatal aspect, so it's actually a pointed cusp which will interfere with the occlusion of the patient so what we do? We reduce it gradually, we remove 1 mm and let the pulp heals and the secondary dentin forms and after 2 months we remove another 1 mm and so on. BUT why we don't remove it at one time? Because it contains pulp tissue so we will expose the pulp.
8-taurodontism: It's enlargement of pulp chamber at the expense of the root. (وعلى )قولة الخصيب خصر ساحل The syndromes which are associated with taurodontism: Ectodermal dysplasia: Tricho-dento-osseous syndrome.
Klinefelter syndrome. Amelogenesis imperfecta.
What's hard about this? If this tooth get infected and you want to do RCT it's a BIG problem because the bur have to go deeper than the level of the bone in order to gain access. So if you find this early enough on an OPG, seal the fissure of that tooth and protect it as much as possible and worn the patient if any thing goes wrong with that tooth properly it will not be manageable and thus they will go to a specialist who's very expensive. **some times the pulp tissue enlarged at the expense of dentine & enamel, and that occurs especially in cases which involve the dentin in the pulp, you can call them cousin ( )زي ولد العمanything goes wrong with the dentin the same thing will affect the pulp, like these cases which affect both of them: • Vitamin D resistant rickets (VDRR). • Vitamin D dependant rickets (VDDR). • Hypophosphatasia • Dentinogenesis imperfecta. • In some cases regional odontodysplasia. These teeth are very fragile it's very easily for microorganism to cause caries and then inflamed the pulp even a simple wear will cause pulpal inflammation and abscess, so that's why you will hear about spontaneous abscess in these patients.
9-enamel chronological defect: Ola said"
"here I'll write exactly what dr.
This is due to environmental causes. **could be quantitative (hypoplasia) or qualitative (hypomineralization). **clinically: manifest as discoloration opacities & enamel hypoplasia. **could be localized or generalized. **Extrinsic staining: It's caused by chromogenic bacteria which produce byproduct causing discoloration to the tooth. You can see black staining, orange, and red one, these can be removed by tooth brushing, prophylaxis or by scaling. **Enamel hypoplasia **Cheese molars like in MIH they look like cheese. **Enamel hypomineralization and opacities.
**Amelogenesis imperfecta. **Dentinogenesis imperfecta: the color of dentin in this condition is grayish or bluish. In most cases of dentinogenesis imperfecta the pulp gets constricted and calcified **Dentine dysplasia: 1-radicular type: the dentine of the root portion is affected, it's short and thin. 2- Coronal type: It affects the coronal portion. **VDRR: rickets is a type of vitamin D deficiency. So it's a defect in mineralization (because there is a defect in calcium & phosphate) the matrix of the bone "ostoid" deposited but it wasn't mineralized. VDRR: genetic type of rickets It's X-linked familial hypophosphataemia rickets. ** X-linked: the gene that causes this rickets is carried on the X chromosome. ** Familial: it exists in families. ** Hypophosphataemia: decrease in blood P, even if you give the patient supplement.
BUT WHY? Because this genetic disease affect the kidney causing a failure of the distal tube in reabsorption of P so all the P will be eliminated in he urine. **so the p will have hyperphosphaturia & hypophosphataemia. Why there is a defect in calcium & phosphate? There are many causes for rickets: Vitamin D deficiency which is important for absorption of Ca & P from GIT. Absorption problem in the intestine which will not absorb nutrients. Or any thing wrong with the cycle which Vitamin D goes through. Malfunctioning kidney because it's very important for both of them, if the level of Ca & P is high it will get rid of this high amount but if they are less than normal it will reabsorb every molecule back to blood stream The hormones that control Ca & P like parathyroid and calcitonin hormones, so any problem in these hormones will affect them. The enzymes that control Ca & P like alkaline phosphate (important for build up bone) and acidic phosphate (important for bone resorption).
10-preeruptive intracoronal resorption of dentine (peird): -it is rare 0.6% in population. It's interesting because it looks like caries but it happens before the tooth eruption so you look at the tooth bud on an OPG inside the bone and you can see dentine resorption. There are many theories that explain this, but the most accepted one said: "osteoclast from the bone enter through some sort of leak in the enamel then they go inside and start resorping the dentine and later on you will find macrophages and inflammatory cells and when the tooth erupted the cavity will be hybrid with microorganisms" You can't diagnose this unless you have a pre-eruptive OPG because it appears as caries, even if you took a biopsy from the cavity and send it to the lab they will tell you that this is caries because the cavity will be hybrid with microorganisms. Or you can diagnose them by asking about the time "how long has the tooth been in the mouth?" So what is your differential diagnosis when you see such a tooth? 1- Caries. 2- PEIRD. 3- MIH in very sever cases; the tooth erupted very weak so enamel could break down very soon after its eruption. SO unless you have a pre-eruptive OPG you can doubt it but you can't be sure. Treatment: 1-after it erupts; you can remove it just like any carious lesion and place a filling. 2-in some cases where these cases were discovered early, they do a flap, remove bone, and fill the tooth with GI until it erupts, and then they do a proper restoration.
9 years old patient, she complained from pain of this 36 it looks normal so we took a radiograph. There was radiolucent inside the crown and around the root apex, she had an abscess and that what causes pain for her. Dr said: "this was the only case that even though I didn't have a pre-eruptive OPG I was so sure that this is PEIRD because there was no sign of caries"
11-eruption problems: Dr said: "you have to study them from 3rd year lecture"
1Eruption hematoma. 2Ankylosis of teeth. 3Erosion: is loss of tooth structure through chemicals It's important for you to know about gastro-esophageal reflex disease: the acid of the stomach become regurgitated into the throat very often during the day. It happens in young children and don't realize it as something wrong because they don't complain, so if you have a look to their mouth you will see the entire palatal surface undergo erosion. You see in pedo clinic that many patients have tooth wear, part of it is caused by attrition. Recent studies say that attrition can't happen without erosion, so erosion is very essential component of attrition.
Done
by:
