|Oral patho lec.3
By the name of Allah
Disturbances in dentine structure:
Dentine is as enamel can be affected by local as well as systemic factors.
- Turner tooth where an infection or trauma to a primary tooth affect the enamel structure and dentine of the developing permanent tooth.
- Radiotherapy to a child with developing teeth can affect the structure of dentine.
b.general causes :
* Systemic disanturbces, as a rule there're many diseases that affect dentine structure.
1. Rickets, where there's increase in predentine and hypocalcification with increase in the amount of interglobular dentine which becomes prominent.
2. Hypophosphatemia (depletion of phosphate), increase in interglobular dentine, large pulp chambers, long pulp horns and cracked enamel as a result early involvement of the pulp causes pulpitis in short time.
3. Hypophosphatasia which is a deficiency in alkaline phosphatase enzyme in osteoblast and other cells depositing dentine so there's increase in predentine and increase in interglobular dentine and large pulp chambers.
So there's group of diseases that affect the calcification of teeth and result in the same feature which is hypocalcification of dentine.
4. Juvenile hypoparathyroidism, children with hypoparathyroidism have small teeth, hypoplastic enamel and short roots, prominent incremental lines in dentine, impaired eruption in some teeth, and defects in root formation.
5. Cytotoxic agents, children with cancer receiving chemotherapy may suffer defects in developing teeth including dentine.
** Dentinogenesis imperfecta DI, (we remember amelogenesis imperfecta) where there's genetic disturbance in the development or structure of dentine.
We have different types of DI,
Type 1 - It's associated with osteogenesis imperfecta (OI), so the child has both OI & DI. - genetic mutations in the DSPP gene , and it's autosomal dominant.
Type 3 rare, Isolated in certain races and types like in Maryland in USA (Dr. said we don’t concern about it much)
Type 2 - this is the most important for us that we may see
- It's known as Hereditary opalescent dentine coz the dentine appears shiny (opalescent = shiny) that we see clinically after eruption of teeth.
- Autosomal dominant, but not associated with OI >>> doesn't have any systemic disturbances.
Primary & permanent) )- both dentition are affected
- Teeth after eruption appear bluish in color or yellowish to brownish and seem to be transparent and opalescent so it is easily recognized clinically.
- After a period of time from eruption the color change and become Amper in shape and there's severe attrition in teeth that their level could reach the gum WITHOUT pulp exposure; you can't see the pulp chamber that lead us to think about the interior of the tooth structure and the DI. This is can be clarified by radiograph…
- radiograph: 1. you have teeth with with obliterated pulp chamber and root canals ; you can't see them they are calcified.
2. Short, blunt roots or spiky thin roots if we have multiple roots for the tooth as a consequence become easily fractured.
3. bulbous crown appearance because of severe constriction of the cervical neck and the small roots so that the crown looks large.
- Clinical importance: those patients are commonly susceptible to root fracture , this lead us to think if they can tolerate crowns , bridges or orthodontic TRT.
1. Enamel is normal, coz the genetic defect is in the developing dentine.
2. Normal mantle dentine which is the first layer of dentine below enamel.
3. The rest of dentine is hypomineralized with less no. of dentinal tubules and the ones that exist are irregular, wide and haphazardly arranged (not in the normal direction in relation to the pulp) , often devoid of odontoblastic process >>> they are not sensitive to cold and hot as normal teeth >>> severe attrition happens with no sensitivity .
4. we have learned that amelodentinal junction (ADJ or DEJ) is scalloped … they thought previously in DI this junction become straight so that the attachment between enamel and dentine is less results in easily chipping of enamel from dentine. then, by scanning & electron microscope the found it as normal teeth so the chipping happens to the undermined defected dentine not in enamel!
Clinical notes for DI:
Dentine is hypocalcified & the enamel is normal >>> very hard enamel with underlying soft dentine >>> with mastication forces enamel fractures >>> early exposure to dentine which is hypomineralized >>> severe attrition with no pulp chamber which is obliterated as that for root canals.
On the other hand those patients are less susceptible to caries as a result of rapid attrition so that no/ less chance for caries to form.
We don't put crowns for patients < 18 in age as their pulp chamber is really large, otherwise we end up with pulp exposure, and waiting until full eruption of crowns, but in DI pulp chamber is obliterated >>> no pulp exposure risk , so we can put on their teeth stainless crowns early to protect them against attrition.
*** Dentine dysplasia, less common , autosomal dominent so there's hereditary and family history. It's 2 types:
Type 1: Radicular dentine dysplasia >>> affects the roots, but the crowns are clinically & stucturally normal so clinically teeth appear normal coz u can't see the roots.
Most common type, normal crown seen after eruption.
By radiographs you may misdiagnose it with DI ; short blunt conical or sometimes abscent root, many of these teeth are mobile as a result of very short root,and obliterated pulp chamber and root canals.
How to differentiate it from DI?
1.characterestics feature of dentine dysplasia type 1 is crescent shaped pulp chamber which is very thin .
2.periapical radiolucencies ( more obvious here); there's inflammation and periapical granulomas but you don't see caries thus the inflammation is not caused by caries instead they thought that bacteria come in to periapical area through defected dentine in the roots where there could be cracks.
Histologically, radicular dentine is abnormal while crown dentine has normal structure. We also notice numerous cacified spherical bodies surrounded by undulating dentinal tubules just like water in rivers around rocks, this structure of dentine is called " water streaming round boulders".
Clinical signs & symptoms: because of the shortened roots the initial signs & symptoms are:
1. extreme tooth mobility and premature or early dental loss so children with such teeth rapidly lose them and can't sustain to the proper time loss of teeth happens either spontaneously or by minor trauma; any hit on their teeth can cause loss of it .
2. less frequently, delayed eruption ; because of roots problems there's no normal eruption.
3.radicular strength is reduced exposed roots to fracture during extraction of the tooth so that reminents stays in the patient jaw.
Type 2: coronal dentine dysplasia >>> where roots are normal . in this type primary teeth differ from permenent teeth;
Primary teeth :
Resemble DI in clinical appearance, structure , radiograph and everything as a result you can't differentiate children with primary teeth affected by dentine dysplasia type 2 frome those having DI.
They are distinct from those with DI so initially we can't differntiate when the child is with primary teeth but when he starts to have permenent ones we can notice the difference.
Here clinicaly permenent teeth appear normal in shape, color and structure while the only difference from normal is the shape of pulp chamber and root canals; the pulp chamber is very wide while the root canals are very thin appearing as thistle-tube and sometimes with calcifications in the chamber (pulp stones).
Again those patients initially appear to have DI then after having permenent teeth they appear clinically normal but if you take radiograph for them you'll notice widening in the chamber and some pulp stones with no symptoms, and this is the differnce from DI.
Regional odontodysplasia : called ghost teeth. ****
Unkonwn aetiology, but they thought it's caused by a defect in a vascular supply to a region of the jaw where teeth in that region have no normal development .
Called regional cause it affects group of teeth usually ant. maxilla : central + lateral + canine for ex. ( 3-4 tooth) are affected while the rest of teeth are normal .
Common presentation : the patient have all teeth exept some adjacent in certain region have not yet erupted or they are there but with abnormal shape and the gingiva surrounding them is thick.
If you detect their structure you'll find:
the enamel is hypoplastic and irregular -
-dentine is thin with increase in interglobular dentine (hypocalcified dentine). So both enamel & dentine are affected in addition to the gingiva.
- pulp stones and widely open apices because of abnormal development of roots.
- focal calcification in the dental follicle around the teeth.
By radiograph, you see things looks like teeth so called ghost teeth!
We have a problem in enamel, dentine, pulp, roots, follicle & surrounding gingiva >>> so called odontodysplasia >>> the whole tooth is affected.
We have two problems, either hypocementosis or hypercementosis which are very rare.
a.hypercementosis, increase in cementum and we mean the cellular cementum, so we have to remember sites of cellular cementum and consequently sites of hypercementosis, not all the root is covered by cellular cementum.
As a result of increase in cellular cementum we'll have bulbous root.
1. periapical inflammation, for ex. there's caries in the tooth then inflammation in the periapical region then stimulation of cementum formation.
2. occlusal forces, some teeth that don't have opposing teeth meaning no occlusal forces on it undergow hypercementosis, or if certain tooth was impacted >>> no occlusal forces on it >>> hypercementosis. On the other hand teeth that suffer extra occlusal forces more than normal due to occlusal abnormalities then hyperfunction and hypercementosis.
3. idiopathic … hypercementosis with no known reason.
4 . Paget's disease.
b.hypocementosis, associated with:
1.cleidocranial dysplasia, where cellular cementum doesn't form so that the roots are thin and there're eruption problems with multiple impacted teeth.
2.hypophosphatasia, we passed on before an said that it affects the structure of dentine in addition those patients don't have cementum >>> no attachment with bone >>> very mobile teeth >>> early loss/shedding of teeth for both dentition: primary & permanent .
We have finished disturbances in the structure.
Disturbances in the eruption & shedding of teeth
a.Early/premature eruption, as in the following cases:
1.We have cases of natal teeth, where infant is born with teeth, and neonatal teeth means that by one month after birth infant will have teeth which are the lower central incisors that are mostly affected
Note: primary teeth normally erupt after 6 month from birth.
Those teeth usually are very mobile and the infant may swallow them or they may cause trauma during feeding for the mother or the infant tongue; remember for infant to swallow he needs to push his tongue forward consequently trauma to the ventral surface of the tongue .
Note: The advice always that we should keep them because they're primary teeth not supernumerary ones as much as we can.
2.premature loss of primary teeth for ex. if the time for certain permanent tooth eruption is at 7 years-old and the primary one was lost before this time by 1-2 years then the permanent one could erupt before this time.
3.hyperthyroidism & gigantism, may be all teeth erupt before their time.
b.delayed eruption/retarted eruption:
delayed : took more time to erupt (late)
retarted : didn't erupt at all .
causes could be local or systemic:
1.retained primary; primary tooth is ankylosed (tied) to the bone and closed the way for permanent .
2.crowding, the common cause for ex. the jaw is small>>> can't accommodate all teeth >>> impaction of teeth, mainly wisdom teeth, upper canines, lower second premolars.
3.trauma of gingiva over one tooth >>> fibrosis >>> prevent the eruption.
4.supernumerary tooth over permanent tooth prevent its eruption, or cyst or tumor of bone in the area of eruption so prevent it.
5.trauma for certain region in the jaw delayed teeth eruption there.
For multiple teeth or even all of them in the following cases:
6.hypothyroidism & hypoparathyroidism.
7. nutritional deficiencies, VD deficiency , anemia >>> delayed eruption.
8.down syndrome & cleidocranial dysplasia.
9.premature birth then delayed eruption of teeth.
The most common teeth impacted are third molars.
c.premature loss, causes could be:
1.caries & periodontal disease … the most common cause when extract teeth because of caries or periodontal disease.
2.hypophosphatasia , as we said before no cementum >>> mobility >>> early loss.
3.severe periodontitis in children with systemic diseases like Palmer-Planter hyperkeratosis or hypophosphatasia as we said and juvenile onset diabetes
4. with diseases like cyclic neutropenia, agranulocytosis, VC deficiency (scarpy) or dentine dysplasia as we mentioned earlier in the lecture.
Developmenta disturbances of bone
a.hemifacial hypertrophy/ facial hemihypertrophy, where one half of the face is suffering increase in size, as a result those patients loose facial symmetry.
Significant unilateral enlargement of the face; during face development one part became larger than the other.
Aetiology: increase neurovascular supply for one part on the count of the other.
Associations: thick coarse skin at the side of hypertrophy, hypertrichosis, mental retardation in 20% and increase susceptibility to tumors.
More important, intraorally: unilateral macroglossia, large teeth (macrodontia) at the side of hypertrophy and even early eruption (premature formation & eruption) consequently malocclusion because one side is larger than the other.
Differential diagnosis , we need it cause hemifacial hypertrophy is not the only cause for face dissymmetry, this is can be associated with other diseases like:
Neurofibromatosis … fibrous dysplasia … arterio-venous malformation … hemangioma … lymphangioma.
b.hemifacial atrophy, here the opposite , becareful of the difference ; in hemifacial hypertrophy one part became larger during development ,while in hemifacial atrophy infants born normal then the disturbance happen at the second decade meaning after 10 years one part starts to appeare smaller than the other … this means another difference ; the first disturbance affects teeth while the second one (atrophy) doesn't!.
it's progressive unilateral decrease of the face size and also other parts of the body epsilaterally; if the right side of the face is smaller they notice that the whole right side of the patient might be affected and become smaller.
The onset: first & second decade but mostly the second. Then the dr. show us a child who's 2.5 years-old appearing normal, at 5 years-old the left side appears larger than right side ( actually the left side is normal but the right one is smaller than it should be) then at 11 years-old very obvious left is normal while right is very small.
Aetiology ia unknown.
Associations: hyperpigmentation of the affected side ( skin is darker) and loss of facial hair on that side.
Intraorally: lips atrophy & tongue atrophy on the affected side ( unilateral microglossia) , smaller alveolar bone , delayed eruption of teeth just in case the disturbance happened very early and short roots which depends on the time at which this disturbance stared to know if the crown or roots will be affected or not!
c.cleft lip/ palate , we'll take more details in other courses of orthodontics & surgery. We have cleft lip, cleft palate and sometimes both together:
1.cleft lip, failure of fusion between median nasal & maxillary process during development of the child that may reach the nostril then it's considered complete cleft lip or doesn't reach the nostril and considered incomplete cleft lip.
Complete one is associated with more problems than incomplete as it may affect the underlying bone thus there could be cleft in the alveolar bone and the teeth get affected so more complications.
Males > females , 25% of all cases of clefts ( 25% to be cleft lip alone), 80% unilateral thus 20% bilateral and if unilateral most common on left side (70%).
2.cleft palate, failure of fusion of lateral portions of palate.
The degree is variable; it could be complete or incomplete and sometimes only the uvula is affected .
Females > males , form 30% of cases.
Minor cases of cleft palate such as cleft uvula are common it can reach 1 from 10 in some places and races and it's clinically not significant if only cleft uvula.
In more severe cases more problems and the growth of the maxilla is affected
3.The rest which are 45% of cases are both CL + CP and M > F.
Aetiology is unknown, but there's family history in 40% of CL and 20% of CP, definite cause is not known it could be nutritional factors; deficiencies in certain vitamins, large tongue could prevent fusion of the palate, toxins & infections & stress to the mother, ischemia to the area , alcohol and certain drugs.
Note: you have to look for the answers of the following question:
Most of the CL cases we saw are to the lateral; the cleft is not in the middle.
Median cleft of the upper lip >>> no fusion between the 2 median maxillary process.
Very rare case, lateral facial cleft, could be unilateral or bilateral, extending from the commissure toward the ear resulting in macrostomia (large mouth). It's lesion between maxillary & mandibular processes during development.
Done by: Haneen Hammoudeh