Great work so far team ..... on all the posts. Its been a pleasure reading them and watching your learning.
We are approaching the last 24 hours of our study period. It's time we made a list of some very important facts.
1. List all the most significant histological changes that are caused by:
a. diabetes - (please refer to the articles we used for the last tutorial. )
b. stress - (please refer to the articles we used for the earlier tutorial. )
(these are changes that would have a direct affect on the periodontium)
2. Using diabetes as an example, relate these histological changes to the pathogenesis of periodontal disease. What role do the periodontal pathogens play here? !!!
3. Lastly, if you had 10 minutes to make a diagnosis, what would be the important issues that you would need to consider to come to an accurate diagnosis!
Please try and do this is a summary format/dot points to help you with your last minute revision.
Sophie
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Will have a go at Diabetes, so 1a.
ReplyDelete1 - Function of immune cells (neutro, macro, mono) altered. t/f (therfore, dont know a short cut) Neutrophil adherance chemotaxis and phagocytosis impaired -> inhibits killing of bacteria in pockets increasing perio destruction.
2- macro & mono increase in response to bacteria, t/f producing pro inflam cytokines and mediators eg. TNFa = increase tissue destruction
Mediators (IL-Lb) found in blood and GCF t/f not only local response but systemical relating to glycaemic control concerns
3- Poor wound healing
Hyperglycaemic conditions (persistent unstable BGL)
- inhibits osteoblast cell proliferation and collagen production
- t/f fibroblasts (produce collagen) are susceptible and degraded by pro inflam (MMPs) compromising healing
- and; increase in bone and attachment loss due to decrease bone formation and compromised quality of newly formed bone.
4- Changes in vascular supply
- Hyperglycaemic conditions again result in high levels of AGE -> bind with collagen forming macromolecules in tissues and periodontium.
-> leads to abnormal cell funtion and capillary growth and vessel proliferation compromising nutrient supply to tissue and perio -> increase risk of VEGF (vascular endothelial growth factor)(CYTONES) further inducing poor blood supply.
Additonally macro and mono have AGE receptors t/f inrease inflammatory response of pro inflam cytokines (IL-1b & TNFa)
Hard to 'list' simplify that......
Diagnosis taken from Hirsch and Wolf and Hassell
ReplyDeleteIS IT?
1 - Gingival
2 - Chronic
3 - Agressive (pre-pubertal, juvenile, rapid, refractory)
4 - Perio manifested by systemic disease
5 - ANUG / ANUP
6 - Perio abscess - gingival /periodontal / pericoronal
7 - Retrograde
8 - Developmental - inherited (ie frenum pull, body jewellery etc.)
THEN?
- induced by poor OH -> gingivitis (slight/mod/severe)
- modified by systemic factors, meds, malnutrition, smoking etc.......
IS IT?
localised or generalised
Early - 4 - 6 mm pkts, no furcs
Mod ~50% bone loss, <8mm pkts
Severe - 2/3 bone loss, sign bone loss, furc invovlement
IS IT ACTIVE?
BOP, mobility, CAL, exudate, migration, radiographic evidence of bone loos, erythema, swelling, oedema????
Also take into account the entire oral environment
ReplyDeleteST, HT, Diet, Lifestyle, Meds, OH
So HT ensure a caries risk assessment is considered
As far as i know, you cannot determine whether perio is currently active (periods of remission), you can only determine whether or not it has been active through accurate radiographs, perio-probing etc. - from Dr. Hirsh's lecture somewhere. Please correct me if im wrong.
ReplyDeleteContributing factors (Nield-Gehrig)
Local: Calc, Tooth Morphology, Plaque Retention
Systemic: Diabetes etc
Acquired: Smoking? Vit C (Malnutrition)
Using this inconjunction with what is assessed clinically, can determine diagnoses i.e. mod gen ginv induced by plaque etc.
Cat and Steven you are absolutely correct. It is impossible to judge periods of activity without baseline data to begin with that you can compare readings with. However, if it is aggressive then you can safely say that there is activity based on the fact that the extend of attachment loss is far to severe when compared to age and presence of plaque/biofilm deposits.
ReplyDeleteAwesome work guys. Make sure you remember all this for tomorrow!
Good call Steven.
ReplyDeleteSorry that's my note taking.
CAL (clinical attachment loss) which comes from (perio probing) and radiographic evidence of bone loss are in the list. I guess i should have highlighted these as essential records ;o)
Just on CAL, i always get it confused with pkt depth and recession. So just to clarify
PD = ging marg -> base of pkt (beware of pseudos)
Rec = CEJ -> ging marg
CAL = CEJ -> base of pkt
well done guys... thanks for this very valuable learning resource you g uys have created.
ReplyDeleteSophie