Saturday, July 30, 2011

The Spinal Cord and Spinal Nerves


  • The CNS is wrapped by layers called MENINGES
  • EPIDURAL SPACE: space just outside of the dura mater and within the vertebral foramen that houses the spinal cord and its meninges
  • DURA MATER: outermost of the meninges, it is made of collagen fibers and is therefore a mechanically protective covering
  • SUBDURAL SPACE: not usually a visible space - the arachnoid is in reality inflated right up against the dura mater.
  • SUBDURAL HEMATOMA: blood fills the subdural space and puts pressure on the spinal cord
  • ARACHNOID: a filmy, lightweight layer that, like a spiderweb, has microscopic extensions which gently hold the spinal cord in place
  • SUBARACHNOID SPACE: space between the arachnoid and the pia mater that is full of cerebrospinal fluid (CSF) in which the spinal cord floats - the subarachnoid space is a sort of hydraulic shock absorber for the CNS
  • PIA MATER: the layer that closely wraps the spinal cord (there is no space between the pia and the spinal cord)- contains blood vessels and supplies circulation to the CNS

Meninges can develop tumors called MENINGIOMAS
     - These are always benign tumors, but they can be dangerous or fatal if they start to displace other tissues and disrupt the spinal cord
  • HEMANGIOMA: an abnormal growth of blood vessels that would, if on the skin, is called a Port Wine Stain. May also be found growing in the vessels of the pia mater,and can be dangerous

  • SPINAL NERVES: run in/out of the spinal cord and extend to/from the body
     - Segmental - each nerve controls a segment of the body, or DERMATOME (a “slice” of skin)
     - Near the spinal cord, they branch to form a dorsal root and a ventral root, and then branch more to form rootlets which connect to the spinal cord
     - DERMATOMAL DISTRIBUTIONS: signs that is restricted to particular dermatomes in the skin
- Inflammation and pain in a particular dermatome is characteristic of shingles
- Numbness in a particular dermatome is a clue to a specific disc being herniated
  • CAUDA EQUINA: spinal nerves with roots that are found at the end of the spinal cord, and that extend downward and out through the sacral foramina
     - The nerves are “hanging” in an extension of the subarachnoid space, and are surrounded by CSF
  • SPINAL TAP: a lumbar puncture to draw CSF or to check spinal cord pressure in the safest region possible, the cauda equina

SPINAL CORD

  • GANGLION: cluster of cell bodies outside of the CNS
dorsal vs. ventral can always be distinguished by the “swelling” that is the dorsal root ganglion on the dorsal root just before the dorsal and the ventral roots meet to become the spinal nerve
  • WHITE MATTER: myelinated axons
  • GRAY MATTER: cell bodies

Three classes of neurons make up a REFLEX ARC:
     1. AFFERENT (SENSORY) NEURONS: can generate action potentials and carry a sensation to the CNS
            - bring impulses INTO the CNS
            - All afferent neurons enter the dorsal root
            - These are BIPOLAR type neurons, which have their cell body located in the dorsal root ganglion, and two axons which extend in opposite directions (one out to the extremity and the other to the CNS)
     2. EFFERENT (MOTOR) NEURONS: carry information/commands from the CNS out to the periphery
            - Cell bodies located in the ventral gray horns
            - All efferent neurons leave the CNS through the ventral root
     3. INTERNEURONS: distribute nerve impulses WITHIN the CNS
            - The most complicated type of all neurons; involved in processing
            - Cell bodies located in the dorsal gray horn and axons extend within the spinal
  cord
Reflexes are “hard-wired” as a consequence of the wiring patterns of efferent neurons,interneurons, and afferent neurons.
  • REFLEX ARCS are involved in fast, unconscious, involuntary reactions.
There is more gray matter in areas of the spinal cord where lots of reflexes are occurring
     - Cervical (arms), lumbar (legs), and sacral (bladder, rectum, sex organs) regions of the spinal cord
Syphilis and polio are two diseases that destroy opposite ends of a reflex arc (for instance, one destroys the sensory half, but leaves the motor half unaffected and vice versa). Multiple sclerosis is a disease that destroys the interneurons and thus the connection between the two halves of the arc.


  • TRACT: a group or "bundle" of axons traveling together
     - ASCENDING TRACTS: sensory
            1. DORSAL COLUMNS: the biggest ascending tracts that bring in information from the outside world
                 - Sensory information about the skin and body position
                 - If damaged, there would be a sensory deficit
            2. ANTEROLATERAL SPINOTHALAMIC TRACTS: send information about pain and temperature sensation to the thalamus
     - DESCENDING TRACTS: motor
            1. PYRAMIDAL TRACTS: voluntary muscle movement
            2. EXTRAPYRAMIDAL TRACTS: involuntary muscle movement
RAMUS: a branch off of a spinal nerve (plural = rami)

NERVES:
PHRENIC NERVE: controls the diaphragm and breathing
     - Out of C3, C4, and C5 - this is important because if the neck is broken below C5 then breathing is still possible
     - Right and left phrenic nerves run down between the heart and lungs to the diaphragm
     - breathing pacemaker: electrodes connect to the phrenic nerve
     - Hiccups: unexplained bursts of action potentials down the phrenic nerve cause spasms of the diaphragm
BRACHIAL PLEXUS: controls the arms
     - Out of C5, C6, C7, C8 and T1
     - Extensions of the brachial plexus:
            1. MUSCULOCUTANEOUS NERVE: controls the coracobrachialis, biceps
     brachi, and brachialis muscles
            2. ULNAR NERVE: runs down and behind the medial malleolus of the humerus to the little finger and part of the ring finger
            3. MEDIAN NERVE: controls lots of the flexor muscles of the hand
                 - comes off of the brachial plexus and runs down the middle of the ventral surface of the forearm
                 - carpal tunnel inflammation will put pressure on the median nerve and will cause loss of sensation in most of the hand and will also cause pain
            4. RADIAL NERVE: controls lots of the extensor muscles of the hand
                 - runs down behind the arm and down the extensor surface of the forearm
LUMBOSACRAL PLEXUS: out of L2, L3, L4, L5, S1, S2, S3, S4, and S5
     - Branches to form three nerves:
            1. FEMORAL NERVE: controls the quadriceps
            2. OBTURATOR NERVE: runs through the obturator foramen and controls the adductor muscles
            3. SCIATIC NERVE: the biggest, longest and fattest nerve in the body
                 - controls the butt, hamstrings, and calves
                 - becomes the POPLITEAL NERVE and then the TIBIAL and FIBULAR (Or PERONEAL) NERVES
                 - SCIATICA: pain and/or paralysis down the leg due to inflammation of or lack of circulation to the sciatic nerve


Value of Coronal Scaling and Subgingival Debridement

TERMINOLOGY

Prophylaxis, Oral: The removal of plaque, calculus and stains from the exposed and unexposed surfaces of the teeth by scaling and polishing as a preventive measure for control of local irritational factors. In the clinic this procedure is selected in the treatment of gingivitis in the hope that the gingival will be returned to a state of health or at least will not develop into periodontitis.
Future preventive / recall cleaning will be termed prophylaxes as opposed to maintenance therapy.

Scaling: Instrumentation of the crown and root surfaces of the teeth to remove plaque, calculus and stains from the teeth.

Root Planing: A treatment procedure designed to remove cementum or surface dentin that is rough impregnated with calculus, or contaminated with toxins or microorganisms. The term is in common usage but is not favored at the UW because it is restrictive, referring only to the root surface and not the adjacent soft tissues.

Root Curettage: Scraping or cleaning the walls of a cavity or surface by mean if a curet.
The procedure not only addresses the root surfaces but also focuses on the soft tissue of the periodontal pocket, especially when sharp, double-edged curets are used. In the patient with periodontitis (as opposed to gingivitis), the student and supervising Periodontics instructor will design a treatment plan consisting of from between 1 to 4 quadrant- equivalents of root curettage depending on the severity of the case. Once this treatment of periodentitis has been selected, then future recall treatment will be termed maintenance as attempts are made to maintain the status quo and prevent further breakdown of the periodontal support. Unfortunately this term is not widely used because many people consider it a surgical procedure.

Subgingival Debridement (SD): The removal of inflamed, devitalized, or contaminated tissue or foreign material from or adjacent to a lesion. This descriptive term for  “ subgingival cleaning” is favored by the UW Department of Periodontics.

Note:  A prophylaxis and quadrants root curettage cannot both be treatment planned on the same patient at the same time.

Benefits and Limitations

During the 1960s, it was shown that supragingival plaque accumulation led to gingival inflammation. It also is generally accepted that pathogenic subgingival plaque cannot develop in the absence of supragingival plaque. Furthermore, changes in supragingival plaque can induce changes in subgingival plaque. Successful periodontal therefore depends on meticulous daily removal of supragingival plaque by the patient and removal of plaque (and probably calculus) by debridement og the crown and root surfaces of the tooth by dental personnel. Both are fraught with problems. Patient compliance usually is not ideal and access to deep periodontal pockets and furcation invasions is difficult, if not impossible. Waerhaug (J Periodontol 49:119,1978) and Rabbani et al (J Periodontol 52:119,1981) demonstrated that SD was fairly effective in removing subgingival deposits in shallow pockets. In pocket depths between 3-5 mm the chances of failure exceeded the chances for success. When pocket depth surpass 5 mm or if significant furcation invasion existed, the chances for failure dominated.

All is not lost! In spite of these limitations there is ample evidence of benefit – at least short-term benefit.

Clinical Studies:
In a 4-week study Morrison et al (J Clin Periodontol 7:199,1980) looked at the effects of OHI, S/SD and occlusal adjustment performed on 90 patients each of whom had at least 20 teeth. The treatment took 4-6 visits. Importat results are illustrated in the following figures.


Results do depend on the degree of inflammation in soft tissue. After 4 week there was a decrease in probing depth and a decrease in periodontal attachment loss in moderate to deep periodontal pockets.  Of equal importance was the slight loss of attachment after instrumentation in shallow pockets. Let the tissues do the talking. In the absence of gingival inflammation, increased probing depths, and calculus, the clinician should be cautious and avoid subgingival instrumentation. “If it ain’t broke, don’t fix it!”

Histologic Studies:
In a clinical / microscopic study in 22 patients, Tagge et al (J Periodontol 46:527,1975) gave OHI and per formed SD and in a site that displayed the same amount of gingival inflammation clinically as another area in the same mouth which was not treated – i.e., the control site. A third similar site was treated by OHI alone. Eight weeks later all 3 sites were assessed clinically for inflammation and 66 biopsy specimens were taken. Clinically and microscopically there was less evidence of inflammation in the SD + OHI sites than in the other two. The data are presented graphically below.


Stahl et al (J Periodontal 42:678,1971) conducted a study to ascertain how long it would take the histologic improvement seen in gingival inflammation as a result of SD to return pre-treatment levels. Eighty suprabony pockets averaging 4.6 mm depth were curetted and then biopsied at appearing specimens from the same patient. By 8 weeks the inflammatory infiltrate was similar in distribution and degree to the control specimens.

Microbiological Studies:
Subgingival debridement has been shown to alter the subgingival microflora purportedly associated with the development of periodontal disease. But for how long? Magnusson et al (J Clin Periodontal 11:193,1993) studied the recolonization of spirochetes and motile rods following SD. The total counts and percentage of these organisms dropped immediately after treatment. By 4 weeks a gradual increase was noted and by the examinations conducted at 8,12, and 16 weeks post- treatment the motile segment of the subgingival microbiota had approached baseline. In a similar study by Handleman and Hess (J Dent Res 49:340,1970) repeated bacterial samples were evaluated after SD at day 3, 10, 30 and 60. There was an immediate increase in Gm + cocci and a decrease in the more complex organisms. The various bacteria studied returned to baseline levels by day 60. Interestingly probing depth was not correlated to the degree of inflammation.

Extended Studies:
()  Badersten et al (J Clin periodontal 8:57,1981 and 11:63,1984) investigated the effect of SD on moderately advanced (4-7mm) and severely advanced (>7mm) periodontitis. In both studies only single-rooted teeth were treated and assessed. The common format included repeated OHI for at least 3 months followed by aggressive SD (with either hand instruments or ultrasonics) every three months until 1 year. The advanced study continued for a second year during which time OHI was given and the teeth received a coronal polish every 3 months. Plaque index, bleeding on probing, pocket depth all improved during the first few months and then remained stable. The results for periodontal attachment level were mixed. In the moderate study there were 106 sites that initially measured at least 6 mm. At 7 months there were 11 such sites and at 13 months there were 13. The advanced study had 305 sites initially measuring at least 7 mm; there were 43 such sites by 24 months. Thus the investigators were able to improve and maintain the periodontal status for 13 to 24 months. It took careful and repeated OHI in a motivated group of people. It took several rounds of thorough SD during the first year and in the second study periodic OHI and coronal polishing for the next 12 mouths. Not to be overlooked is the fact that all teeth were single-rooted. Molars, especially those with furcation invasions, really complicate treatment. May require surgical access to cope with problems.

()  In an excellent long-term clinical study by Kalkwarf et al (J Periodontol 59:794,1988) a variety of surgical and non-surgical modalities were compared in teeth with furcation invasions. Regardless of the method used all sites tended to breakdown in the second year of maintenance.

()  Fleischer et al (J Periodontol 60:402,1989) demonstrated that in molars with furcation invasions and probing depths of at least 7 mm, the percent  of attachment loss in the furcations was over 3 times the percent of loss on external root surfaces. That’s ugly!

Summary:
In spite of the limitations of access, especially in the posterior of the mouth and in the presence of furcation invasions, careful SD will lead to clinical, histologic and microbiologic improvement in moderate to severe periodontal disease – at least over a 2-3 month period. The better the patient’s plaque control efforts, the better the results, and the longer they will last.
Subgingival debridement is not advised in healthy sulci.


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Disorders of Teeth other than Dental Caries

·         Eruption and Shedding
·         Non-Bacterial Loss of Tooth Substance  
·         Discoloration of Teeth
·         Transplantation and Reimplantation
·         Root Fracture
·         Age Changes     


Disorders of Eruption and Shedding

Premature eruption , Natal and Neonatal teeth :

Natal and Neonatal teeth:

·         Premature : before the proper time
·         Usually teeth start to erupt at the age of 6 months + or - , and sometimes as early as 3 months . It might be delayed as well, to the age of 9,12month.some neonate (new born) are born with teeth or start to erupt shortly after birth . these teeth are called :
·         Natal - if present at birth
·         Neonatal - if erupted shortly after birth
·         80% of these teeth are the mandibular incisors .

      Remember: the first teeth to erupt are the mandibular incisors, so common sense .

  • Due to this premature eruption there is lack of root formation, and the mobility during eruption might lead to irregularities in its structure (it is still developing) leading to premature loss .
  • we might extract them before they are lost if :
      • we are scared that the infant might inhale them
      • they are causing ulceration to the opposing oral mucosa
      • they are causing injury to the mother while nursing
  • If we feel that they are stable we can provide them with covering plate
  • While nursing rather than extraction.

 Local Factors for Other Teeth:
Such as premature eruption of permanent teeth (which is widely seen in our population) as a result of :
Dental caries of deciduous teeth and lack of oral health education, which might lead to malocclusion as well - premature loss of deciduous teeth
Superficial location of tooth germs in the jaws

Endocrine abnormalities:
  • lead to generalized premature eruption
  • such as increase in GH and hyperthyroidism
 Remember:
             Increase in GH in children - gigantism
             Increase in GH in adults    - acromegaly
Retarded Eruption :

General causes:

·         Such as :
o   Hypothyroidism : leads to cretinism
o   Prematurity : born earlier
o   Nutritional deficiencies
o   Chromosomal abnormalities
 Local causes:
·         When permanent teeth (as well deciduous but less common) have got the eruptive force but there is sth preventing them .
·         it could be :
o   Idiopathic
o   Migration & traumatic displacement of tooth germs
                                                      
·         As if a child was exposed to a trauma that moved his tooth germs far in the jaw or to become impacted by other teeth
·         Abnormally large crowns : can’t find space for eruption

Delayed Eruption and Multiple Supernumerary Teeth:

  • Any condition which have multiple or even single supernumerary teeth might obstruct the track of chronology , 
  • Or the supernumerary teeth itself can’t erupt .
  • Such in Cleidocranial Dysplasia : a condition associated with :
      • Total or partial absence of the clavicles
      • Cranial sutures abnormalities
      • Hemifacial hypoplasia
      • Depressed nasal bridge
      • Multiple impacted supernumerary teeth

Premature Loss :
·         causes :
            1-dental cries and its sequelae* - such as pulpitis 
            2- Chronic periodontitis *
            3- Aggressive periodontitis

·         Periodontitis is an inflammation that start with gingivitis and progress to the periodontal fibers and the alveolar bone .
·         There is a variant of periodontitis that isn’t related to poor oral hygiene - aggressive periodontitis
               
            4- Hypophosphatasia
            5- Papillion-lefèvre syndrome - also known as palmer planter Hyperkeratosis

                   * The most common causes dental caries + periodontitis
  
Persistence of Deciduous Teeth :

  • it is also termed as : retained or submerged deciduous teeth
  • the condition in which deciduous teeth don’t shed at the time they should
  • A case for eg. is : when the development of the successor teeth is retarded, so it won’t erupt and the deciduous will persist in the mouth
  • Another eg. is: when there is a congenitally missing permanent teeth the deciduous may remain in its position .

      • so persistence of deciduous teeth result from failure of eruption of  permanent successor because it is missing , displaced or lack formation
A generalized condition is found in cleidocranial dysplasia  .
  e) Impaction of Teeth:

  • A very common eg. is 3rd molar impaction due to lack of space
  • Other teeth might be affected such as : maxillary canine , mandibular 2n premolar .
  • Impacted teeth : teeth which remain unerupted or partially erupted beyond the expected time 
  • It might affect 1 or more teeth
  • It might be symmetrical : on the Rt + Lf or in the upper + lower
  • Is rare in deciduous
  • When a tooth is partially erupted it might cause problems :
The gingiva is opened to the oral cavity - accumulation of food and debris
-          hard to clean - caries , periodontitis or any source of infection 
  • it might cause resorption in the adjacent tooth
Local causes:
             1-Abnormal position of germ Æ too far in the jaw
             2-Lack of space Æ such for 3rd molar and maxillary canine
             3-Supernumerary teeth Æ such in cleidocranial dysplasia
             4-Cysts (odontogenic tissues are capable of forming them)
             5-Tumors(odontogenic tissues are capable of forming them)
             6-Cleidocranial  dysplasia

Complications:
             e Resorption of impacted or adjacent teeth
             e Formation of dentigerous cyst
·       Dentigerous cyst :is a developmental cyst around the crown of impacted teeth that result from the accumulation of fluids between the enamel and residual enamel epithelium
             e Formation of odontogenic tumors

 f Another term is embedded teeth : teeth which remains unerupted due to 
Lack of eruptive force in the absence  of a physical barrier 
Remember: impacted - physical barrier 
But usually people use impacted for every thing.
      
f) Reimpaction of Teeth :
      
     f Occur when the alveolar process doesn’t grow enough and the tooth become ankylosis with adjacent bone.  

Ankylosis : the union of 2 bony structures .Cementum is similar to the bone structure.

Remember: the alveolar processes of the deciduous teeth grow to accommodate the size and length of the permanent teeth and to reach the correct occlusion.
  
  •      As a result there is absent of PDL fibers in that aria 
  •      Also known as infraocclusion  or submerged teeth
  •      Called reimpaction because it is infraocclusal (impacted from the normal occlusion)  
  •      In some situation neighboring teeth tilt over affected tooth, and it may be completely covered by mucosa
  •      Mostly affects the deciduous mandibular 2ed molar lacking a successor 2ed premolar


Non Carious Tooth Substance loss
Attrition :

·         wearing away of tooth substance during tooth to tooth contact- during grinding of teeth against each other
·         it is a slow physiological process that appears more in elderly
·         might be accelerated by abrasive foods
·         pattern:
§  incisal edges of incisors,
§  occlusal surfaces of molars,
§  palatal cusps of maxillary teeth,
§  buccal cusps of mandibular teeth

You might be surprised of the presence of Approximal attrition on the proximal surface results from the movement of PDL fibers during eating ,talking,…etc so the contact points become flat as a result teeth tend to slightly move toward the mid line – mesial migration
   
     f More pronounced in males
     f Abrasive food property affects the rate 

     f Pathological attrition may result from
            1- Abnormal occlusal relationship
            2- Bruxism and habits such as tobacco and betel chewing
            3- Abrasive dust particles - consist of silica
            4- Abnormal tooth structure such as amelogenesis imperfecta and
                dentinogenesis imperfecta - weakness of the structure

 f Exposed dentin becomes discolored yellow to brown and it becomes attritic faster than enamel, cause it is softer, creating cup-shaped defects or wear facet
     f Formation of reactionary dentine protects pulp
     f And there is formation of dead tracks and translucent zones.

Abrasion :
  • pathological wearing away of tooth structure due to repetitive friction of a foreign body
     f Examples:
           1- Nuts and million seed abrasion
           2- Toothbrush abrasion
      • due to roughness and poor technique
      • brushing motion should be vertical + circular with a smooth brush
           3- Habitual abrasion in pipe-smokers
           4- Occupational abrasion e.g. hair-grips, nails, musical instruments
           5- Ritual abrasion - related to certain tradition

Abfraction :

Loss of tooth structure that results from repeated tooth flexure caused by occlusal stresses
Flexure: blending
     f enamel tend to blend to some extant at stress then it will fracture
     f while dentin is able to withstand greater tensile stress than enamel
     f When eccentric occlusal forces are applied to a tooth, tensile stress is concentrated at cervical fulcrum, leading to flexure that may produce enamel cracks
     f Cracked enamel can be lost or more easily removed by erosion or abrasion

Erosion :

     f loss of tooth structure resulting from chemical action (acid action)

Dietary erosion :

     f Excessive intake of acidic beverages or sucking of citrus fruits- palatal surfaces of teeth and labial surfaces of maxillary incisors

Occupational erosion:
   
  f e.g. battery factories- labial surfaces of maxillary and mandibular incisors

Acid reflux or chronic vomiting:

  f e.g. anorexia, bulimia nervosa, chronic alcoholism as well in hernia

Idiopathic:
 Resorption :
   
    f Usually the root resorp but sometimes the crown resorp as well such in impacted teeth

Physiological resorption:

    f Is seen in the root of deciduous teeth prior to shedding

    f Sometimes it occurs as a result of permenant teeth movement and called transient resorption

    f Transient microscopic areas of superficial resorption of roots of permanent teeth, repaired by cementum or bone-like tissue apposition
  
Pathological resorption :
    • External - start from the root surface
    • Internal - start from the pulp
The cells of action are osteoclast or might call them odontoclast

    1- External resorption :
     f Might be associated with: Periapical inflammation
     e Results from the progression of dental caries , pulpitis , pulpal necrotic tissues through apical foramina
     e Inflammation might cause - bone resorptionroot resorption excessive mechanical force e.g. improper orthodontic treatment
     e Orthodontics is based on the movement of teeth resulted from the resorption and deposition of  bone
neoplasms or cysts transplanted or replanted teeth
     e Transplantation: the placement of a tooth in an another socket
     e Reimplantation : the placement of the lost tooth in its own socket idiopathic, burrowing type in cervical area - no known cause
Crowns of impacted teeth

    2- Internal resorption :
      f Occurs from the pulp chamber to the outside
      f The clasts originate from it and we call them dentinoclasts 
      f So a vital pulp is needed
      f May be:
Secondary to pulpitis
Idiopathic
      f Clinically we start to see the pulp through enamel - pink tooth or by a radiograph
                   Remember: pink because it is vascularised

Discoloration of Teeth
    By:
            a) Surface deposits - extrinsic staining such as smoking , coffee , tea
            b) Changes in the structure or thickness of the dental hard tissues
            c) Diffusion of pigments into the dental hard tissues after their formation
            d) Incorporation of pigments into the dental hard tissues during their formation

What is the difference between pigments and stains ?
  • Pigments : produced by the body
  • Stains : are extrinsic
Extrinsic Staining :

      f Causes:
              1- Foods and drinks - usually transient
              2- Chromogenic bacteria- pigment producing bacteria
                e Teeth apperes dark brown to black and they are usually caries resistance
                e But these stains are usually hard to remove
Topical medications and mouth rinses
Tobacco products
  
 b) Changes in Structure or Thickness of Dental Tissues :

      f Any abnormality in dental tissues
      f Causes:
              1-Dental caries
              2-Enamel hypoplasia: e.g. fluorosis (environmental), amelogenesis
                    imperfecta (hereditary) , enamel opacities
              3-Dentinogenesis imperfecta
              4-Dentinal dysplasia type II
              5-Age changes

c) Diffusion of Pigments into Dental Tissues After Formation :

   f At this stage the tooth isn’t vital and you can till from its appearance
   f Examples:
          1- take up of food & tobacco stains by exposed dentin
          2- restorative & endodontic materials : amalgam sometimes stains
          3- Pulp necrosis

Incorporation of Pigments into Dental Tissues During Formation :

  f Examples:
          1- Congenital hyperbilirubinemia - neonatal jaundice - green to yellowish brown
          2- Congenital porphyria - pinkish-brown - red fluorescence under UV light
          3- Tetracycline intake during pregnancy or childhood - yellowish changing into brown
                     eThe most important
                     eInfant deciduous and maybe first molars become stained
                     eSo it is contraindicated to prescribe this antibiotic in pregnancy and childhood conditions

Transplantation and Re-implantation
   
     f Reimplantation :
             eReturning a tooth to its socket after avulsion.
             eSupposing a child while running has lost his incisor if we try to re-implant it within an hour , and we’ve already preserved it in milk
               (Body temperature), then the process might success .
    f Transplantation:
             eTransfer of a tooth to another location in the jaw
             eIt is rarely done
             eSupposing that some one has lost his 1st molar it could be replaced by for e.g. his 3rd molar

    f Both are associated with resorption
    f Other complications:
          Loss of pulp vitality, failure of root completion, poor periodontal healing

Root Fracture

    f As a result of trauma
    f Occur at different levels of the root
    f The outcome depends on :
             1-presence or absence of infection - if the gingiva is opened or the tooth is carious there might be failure
             2-vitality of pulp
 Position of fragments - it is better when it is more toward the apex
 3-degree of comminution

 4-Location of fracture
 5-Mobility of coronal fragment

   f Pattern of healing:
                 1- Fragments become united totally or partly by calcified repair tissue - such as cements
                 2- Fractured surfaces become rounded off and clothed by cementum with formation of fibrous tissue in between
                 3- Fractured surfaces become rounded off and clothed by cementum with formation of fibrous tissue and bone in between

Age Changes

  a) Enamel become:
                  1- More brittle -more cracks
                  2- Less permeable
                  3- Darker

  b) Dentine:
                  1-Continued formation of secondary dentin with reduction or obliteration of pulp chamber
                  2-Continued formation of peritubular dentin results in transluce dentin
                               e The increase in thickness around the tubule results in this translucency
                  3-Roots become brittle
                                e So becoming thicker doesn’t mean becoming stronger
          
  c) Cementum :
                  1-Continued formation and increased root thickness
                  2-Hypercementosis in presence of other causes

In general if you look at an old tooth you’ll see:
  • Narrowed pulp chambers and maybe some calcified portions
  • Tertiary dentine
  • Enamel cracks
  • Gingival ressetion      

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