Clinical and histological responses to non-surgical therapy Flashcards
Give 6 reasons why we review patients gingivae health post treatment.
- Evaluate response to treatment
- Improve patient involvement
- enquire about patient-reported outcomes
- increase pateient awareness
- revise treatment plan if necessary
- provide short, medium and long tern aind of treatment
What 5 things do we assess in a full periodontal reassessment?
- Pocket probing depths (including BOP)
- Recession
- Mobility
- Furcation involvement
- Plaque control
Give 3 good predictors of periodontal health.
- Absence of plaque
- Absence of bleeding
- Absence of pocketing
Give 6 responses to periodontal treatment.
- Lack of bleeding
- Pocket reduction
- Clinical attachment level gain
- Recession
- Sensitivity
- Patient does not report with complaints and is happy with OH regime.
Why before periodontal therapy are probing depths high?
- Calculus attracts biofilm
- This biofilm causes inflammation.
- Leads to unstable connective tissue so the probe can reach further depths.
Why does recession occur after periodontal therapy?
As inflammation goes down so gums recede.
If periodontal therapy is sucessful what are 4 visible changes you will see?
- Gingival tissue texture (from spongy to firm)
- Contour (from swollen papillae to the flattening of soft tissues, scalloping and stippling of attached gingivae)
- Colour (from red gingivae with bleeding on probing to healthy pink).
These are all positive signs that there has been an overall resolution of inflammation
What are the 3 classifications for site specific responses?
- Treated
- Responding
- Non-responding
What do we do at a clinical endpoint with a perio patient?
Patients will usually enter a period of supportive periodontal therapy.
What are 3 signs a site specific area is ’responding’?
- Reduction in pocketing
- Absence of bleeding
- (Absence of plaque)
What is the next step for a ‘responding’ site?
- Non-surgical therapy as there is now more space to access.
- Possibly surgical
What are 3 signs a site specific area is ’non-responding’?
Persisting inflammation
Persisting or increasing pocketing
Persisting or increasing symptoms
Give 3 reasons for suboptimal outcomes with site specific responses.
Patient factors (e.g. systemic conditions, poor compliance/motivation, inadequate plaque control, smoking)
Site factors (e.g. restorative status, endodontic pathologies, type of osseous defect)
Operator factors (e.g. level of skill, time for treatment, inadequate debridement, incorrect diagnosis)
Give 5 steps to remedy suboptimal outcomes with site specific responses.
- Review modifiable systemic risk factors – smoking status, diabetes control, medication
- Evaluate oral hygiene – provide patient-specific advice
3.. Evaluate restorative status of the tooth – examine for cracks, fractures, overhangs, fremitus
- Consider antimicrobials – for well-motivated/engaged patients
- Consider periodontal surgery – to regenerate or eliminate lesions that add complexity (e.g., intrabony and furcation lesions)
Repeat NSPT (Non-Surgical Periodontal Therapy) – for non-responder sites in engaged patients (surgery is not usually done after a single phase of NSPT)
What are the histological lesions in initial gingivitis (24-48 hours)?
Localised to gingival sulcus and subadjacent periodontal tissues.
Local vasodilation bringing IgG, complement fibrin and more PMN into the tissues
Increased GCF.
PMN migrate into the gingival crevice via the junctional and sulcular epithelium
few lymphocytes and macrophages are evident in the junctional epithelium
serum antibodies to plaque antigens previously encountered are detectable: immune complexes can form activating the classical complement cascade to produce C3a and C5a. Both will increase vascular permeability and all chemotaxins for PMN
What are the histological lesions in early gingivitis (4-7 days)?
Localised proliferation of junctional epithelium and sulcular epithelium
greater increase in GCF
PMN still present in the crevice and with the periodontal tissue
local accumulation of lymphocytes most of which are T cells
Circulating lymphoid cells may traffic to the gingival inflammatory focus and may release cytokines which promote further lymphocytic infiltration and proliferation
What are the histological lesions in established gingivitis (2-3 weeks)?
proliferation of junctional epithelium and sulcular epithelium some loss of collagen but no loss of attachment
New vessel formation: plasma cells are found adjacent to the vessel an gingival lesion there is mainly IgG and IgA but very little IgM present.
Maximum increase in GCF
PMN persist
T cells dominate the lesion
by this stage lymphocyte proliferative responses to plaque antigens are evident. There are also non specific polyclonal b cell mitogens. B cells may see to the local gingival inflammatory focus and therefore provide a source of plasma cells and IgG, IgA and IgM.
What are the histological lesions in advanced periodontitis?
Pocket formation loss of attachment collagen and bone loss. And imbalance in the host- microbial interaction heralds the transition from a successful defence to a destructive pathological reaction. There is also a reparative fibrotic response which becomes more evident with time.
establish lesion with more IgM.
Gcf IgG, IgA, IgM and complement
PNM persist
Dense infiltrate of lymphocytes, plasma cells on macrophages. The breakdown in the epithelial barrier [pocket lining) will allow plaque antigens direct access into the periodontal tissues and activate immune cells. This in itself could lead to a bystander damage and further tissue damage.
The presence of IgG, IgA, IgM and complement and emphasise would suggest that there is a potential for type IV cell mediated AND type II and type III antibody antigen reactions that may lead to tissue damage. The important bacterial antigens are however not known and nor do we know precisely what the lymphocytes are doing in this chronically inflamed periodontal tissue
What are the 3 microbiological changes to the biofilm when you carry out non-surgical therapy?
Major disruption to the biofilm
Shift from predominantly anaerobic to predominantly aerobic flora
Reduction in total number of organisms
What are the 2 cellular responses to non-surgical therapy?
Initial acute inflammatory response
Initiation of resolution of inflammation
Name 5 things present in a periodontal pocket in an advanced lesion.
subgingival calculus and plaque
inflammatory infiltrate extending into the connective tissue
ulcerated pocket lining
alveolar bone loss
loss of attachment
Name 5 changes in a periodontal pocket one week post non surgical therapy.
number of neutrophils in pocket decrease
inflammatory infiltrate decreases
ginigival swelling decreases
pocket lining begins to heal
increase in fibroblasts
Name 4 changes in a periodontal pocket one month post non surgical therapy.
Continued reduction in inflammation
Formation of new gingival connective tissue
Reattachment of pocket epithelium → formation of long junctional epithelium
Mature gingival connective tissue with few inflammatory cells
Evidence of bone remodeling at the alveolar crest (but no coronal regeneration)
Why does pocket reduction occur post non surgical therapy?
As inflammation subsides.
