Gum Drop Technique (GDT)
[Gingival recession; PRP; L-PRF; A-PRF; i-PRF; Fibrin clot]
1. If PRP could promote simultaneous tissue regeneration as well as alveolar bone repair – towards restoring extraction sockets or implant site development or ridge augmentation for defect correction, then, are you sure that patient’s blood derived plasma-rich fibrin (PRF / leucocyte- and platelet-rich fibrin L-PRF) would do justice towards alveolar bone repair (with maximum success rate), even though, the complex fibrin matrix of L-PRF’s autologous platelets and leucocytes tend to accelerate the healing of soft and hard tissue?
OR
Is it due to the abridged preparation of PRF in the absence of the requirement on biochemical blood handling?
2. What is the basis for concluding that PRF would ‘always’ turn-off the localized inflammation by acting as an immune regulation node with inflammation retro-control ability?
3. Irrespective of an individual’s medical history, whether, PRF would always accelerate the healing in the absence of any detrimental effect on the quality of the resulting bone and would it always lean to an enhancement in overall osseous regeneration and soft-tissue healing?
4. Under what circumstances, the concentrated fibrin fails to behave as a tissue glue (holding hard-tissue graft material together into a moldable material) and eventually failing to adhere to the underlying bone and overlying soft tissue?
5. In the context of enhancing soft-tissue healing associated with the treatment of gingival recession, how exactly advanced-PRF (fibrin clot deduced from centrifuged blood @ 1300 rpm/8 min, which becomes a membrane, and which gets replaced with autogenous connective tissue or acellular membranes) remains inferior than the injectable-PRF centrifuged @ 700 rpm/3 min?
Do we have a control over the release all the growth factors that gets released?
What exactly induces an enhanced fibroblast migration?
If low speed and low centrifugation concept remains responsible for changing the fundamental dynamics of the fibrin clot, whether reducing further from 700 rpm / 3 min – would really enhance the number of cells, vessels and matrix by enhancing the growth factors, cytokines and fibronectin?
6. Albeit, GDT involves biologically enhanced soft-tissue procedure, while comprising the aids of an autogenous graft material, how minimal the invasive would remain to be?
7. How do we ensure a normal regeneration (that requires cell death) that follows a proper direct growth – upon applying GDT Technique?
What if the growth factors released from platelets and leucocytes within A-PRF & i-PRF fail to stimulate new blood vessel growth through VEGF and FGF; and in such cases, how do we expect the new attachment of the gingival tissue to the root surface?
Can we still end up with a stable attachment?
Suresh Kumar Govindarajan
Professor (HAG) IIT Madras
https://home.iitm.ac.in/gskumar/
https://iitm.irins.org/profile/61643
27-July-2024
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