Dentin dysplasia (DD) is a rare hereditary disturbance is inherited as an autosomal dominant trait.
unknown etiology that affects approximately 1 :100,000.
In 1972, Witkop classified it into type I and type II which affect both dentitions.DD Type I
Radicular dentin dysplasia
Characterized by:-
1.Both dentitions are affected.
2.Normal appearing crowns
3.No or only rudimentary root development (rootless teeth)
4.Incomplete or total obliteration of the pulp chamber.
5.Teeth may exhibit extreme mobility and exfoliate prematurely.DD type II
coronal dentin dysplasia
Characterized by:-
1.partial pulpal obliteration.
2.Thistle-tube-or flame-shaped coronal pulp chambers
3. Thread-like root canals
4. Usually the absence of periapical radiolucencies.
5. In this type of anomaly, teeth roots are of normal shape and contour.The enamel and the immediately subjacent dentin appear normal.
Deeper layers of dentin show an atypical tubular pattern with an amorphous, atubular area, and irregular organization.
Normal dentinal tubule formation appears to have been blocked so that new dentine forms around obstacles and takes on the characteristic appearances described as “lava flowing around boulders”The radiograph revealed features of dentine dysplasia type I with normal appearance of crown but no root development Autosomal Dominant Disorder:
Manifested in heterozygous states
At least one parent of index case is usually affected
Both males and females are affected.
Clinical feature can be modified by variation in penetrance and expressivity. Some individual inherit the mutant gene but are phenotpically normal. This is reffered to as “incomplete penetrance”.
In many condition the age of onset is delayed.
Inheritance Pattern:
Typical pattern is a heterozygous affected parent with a homozygous unaffected parent.
Every child has one chance in two of having the disease
Both sexes are affected equally..Autosomal Recessive Disorder
Largest category of Mendelian disorder
Usually does not affect the parent of the affected individual, but sibling may show the disease.
Complete penetrance is common.
Onset is frequently early in life.
Usually affect enzymatic proteins.
Pattern Of Inheritance:
Typical pattern is two heterozygous unaffected (carrier) parent.
The triat does not usually affect the parent, but siblings may show the disease
Siblings have one chance in four of being affected
Both sexes affected equally.
Dentin dysplasia (DD) is a rare hereditary disturbance is inherited as an autosomal dominant trait.
unknown etiology that affects approximately 1 :100,000.
In 1972, Witkop classified it into type I and type II which affect both dentitions.DD Type I
Radicular dentin dysplasia
Characterized by:-
1.Both dentitions are affected.
2.Normal appearing crowns
3.No or only rudimentary root development (rootless teeth)
4.Incomplete or total obliteration of the pulp chamber.
5.Teeth may exhibit extreme mobility and exfoliate prematurely.DD type II
coronal dentin dysplasia
Characterized by:-
1.partial pulpal obliteration.
2.Thistle-tube-or flame-shaped coronal pulp chambers
3. Thread-like root canals
4. Usually the absence of periapical radiolucencies.
5. In this type of anomaly, teeth roots are of normal shape and contour.The enamel and the immediately subjacent dentin appear normal.
Deeper layers of dentin show an atypical tubular pattern with an amorphous, atubular area, and irregular organization.
Normal dentinal tubule formation appears to have been blocked so that new dentine forms around obstacles and takes on the characteristic appearances described as “lava flowing around boulders”The radiograph revealed features of dentine dysplasia type I with normal appearance of crown but no root development Autosomal Dominant Disorder:
Manifested in heterozygous states
At least one parent of index case is usually affected
Both males and females are affected.
Clinical feature can be modified by variation in penetrance and expressivity. Some individual inherit the mutant gene but are phenotpically normal. This is reffered to as “incomplete penetrance”.
In many condition the age of onset is delayed.
Inheritance Pattern:
Typical pattern is a heterozygous affected parent with a homozygous unaffected parent.
Every child has one chance in two of having the disease
Both sexes are affected equally..Autosomal Recessive Disorder
Largest category of Mendelian disorder
Usually does not affect the parent of the affected individual, but sibling may show the disease.
Complete penetrance is common.
Onset is frequently early in life.
Usually affect enzymatic proteins.
Pattern Of Inheritance:
Typical pattern is two heterozygous unaffected (carrier) parent.
The triat does not usually affect the parent, but siblings may show the disease
Siblings have one chance in four of being affected
Both sexes affected equally.
This presentation features the various measures which can be undertaken to prevent pit and fissure caries to develop i an otherwise healthy oral environment. The use of pit and fissure sealants is emphasised in case of deep pits and fissures.
Gingival cyst of newborn /orthodontic courses by Indian dental academy Indian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
DR. SWARNEET KAKPURE (DEPT OF CONSERVATIVE DENTISTRY AND ENDODONTICS)
THE TOPIC PRESENTED IN SEMINAR COVERS ALMOST ALL THE ASPECTS OF COMPLEX AMALGAM RESTORATIONS INCLUDING PIN RETAINED,SLOT RETAINED AMALGAM RESTORATIONS,CEMENTED,FRICTION LOCKED & SELF THREADING PINS, TMS SYSTEM,AMALGAM FOUNDATIONS ALONG WITH TECHNIQUES OF INSERTION AND MATRIX PLACEMENT.
This presentation features the various measures which can be undertaken to prevent pit and fissure caries to develop i an otherwise healthy oral environment. The use of pit and fissure sealants is emphasised in case of deep pits and fissures.
Gingival cyst of newborn /orthodontic courses by Indian dental academy Indian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
DR. SWARNEET KAKPURE (DEPT OF CONSERVATIVE DENTISTRY AND ENDODONTICS)
THE TOPIC PRESENTED IN SEMINAR COVERS ALMOST ALL THE ASPECTS OF COMPLEX AMALGAM RESTORATIONS INCLUDING PIN RETAINED,SLOT RETAINED AMALGAM RESTORATIONS,CEMENTED,FRICTION LOCKED & SELF THREADING PINS, TMS SYSTEM,AMALGAM FOUNDATIONS ALONG WITH TECHNIQUES OF INSERTION AND MATRIX PLACEMENT.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
All of us would love to have a gleaming smile on our face. It usually a result of crystal white beaming teeth. But what will happen when the teeth have a cone-shape and are significantly smaller than average, there might not be that attraction as compared to normal
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Etiology of malocclusion local factors /certified fixed orthodontic courses b...Indian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide range of dental certified courses in different formats.
etiology of malocclusion for general practitioners.docxDr.Mohammed Alruby
Etiology of Malocclusion
For general practitioners
Prepared by
Dr. M Alruby
Etiology in orthodontics is the study of actual causes of dento – facial abnormalities.
Malocclusion is the condition where there is a deviation from the usual or accepted relationship, dental malocclusion exists when the individual teeth within one or both jaws are abnormally related to each other, this condition may be limited to a couple of teeth or involving the majority of teeth present.
Development of normal dentition and occlusion depends on a number of interrelated factors that include the dento alveolar, skeletal and the neuromuscular factors. Thus localization of the possible etiology may be a very difficult task.
A- Extrinsic factors:
1- Evolution:
With evolution, the jaws become smaller, reduction in the number and size of teeth and diminution of jaw projection together with increased in vertical height of the face and there is retrognathic tendency in man as he ascends the evolutionary scale.
2- Heredity:
Transmission of dento facial characteristic through generation by genes. The child is a product of parents who have dissimilar genetic material. Thus the child may inherit conflicting traits from both the parents resulting in abnormalities of the dentofacial region. Another reason attributed for genetically determined malocclusion is the racial, ethnic and regional intermixer, which might have led to uncoordinated inheritance of teeth and jaws.
There are three types of transmission of malocclusion from the stand point of genetics:
1- Repetitive: the recurrence of single dentofacial deviation within the immediate family.
2- Discontinuous: a tendency for a malocclusion trait to reappear within the family over several generations.
3- Variable: the occurrence of different but related types of malocclusion within several generation of the same family.
Dental defect of genetic origin include the following:
= Crowding and spacing of teeth.
= Size and characteristic of soft tissue including muscles and frenum.
= Macrognathia and micrognathia.
= Macrodontia and microdontia.
= Oligodontia.
= Tooth shape variations.
= Median diastemas.
= upper face height, nose height, and bigonial width.
= Bimaxillary protrusion.
4- Congenital:
Those are deformities of hereditary or non-hereditary origin but exciting at birth.
The congenital abnormalities that cause malocclusion:
= Cleft lip and palate:
lack of fusion between the two palatal processes to each other. From one third to one half of all cleft palate children have familial history of this deformity.
As with the non-cleft child, palatal, pharyngeal and perioral musculature is well developed at birth to meet the demand of suckling, deglutition and mastication. While the complete unilateral or complete bilateral cleft break the continuity of the upper lip and disturbs the functional pattern and significantly reduce the restraining effect of the buccinators mechanism that pro
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