these cytokines will increase in situations where the tissue is suffering damage. The compression site is one such location. The periodontal ligament is designed to resist tension trauma so this may have a significant effect upon the tissue stability and ability to resist the trauma.

PDL is designed to resist both the compression and tensional forces, however to a certain extent. During orthodontic tooth movement continuous compression leads to a state of ischemia and stress buildup which intiates an inflammatory reaction wherein cytokines like IL-1; PGE2 and RANKL comes into picture. In the absence of any infection, these inflammatory markers themselves are responsible for causing bone resorption and thus facilitate tooth movement. On the other hand, in tension side the blood vessels are streched and does not comprimize the blood supply. Hence the stress level is minimal which stimulates bone formation rather than resorption.

True. Cytokines are secreted in areas of tissue damage only. The pl recognizes the compression site as more dangerous than the tension side hence the presence of more cytokines there.

During the initial tipping phase (approximately 24hrs), significant compression and the associated ischemia and inflammation initiate the recruitment of chemo-kines and cytokines. Then there is a lag phase during which not much movement occurs, allowing for these to arrive at the site where bone resorption will occur (and the subsequent movement of the tooth thru the bone). There is not a continual state of severe compression or ischemia associated with the low forces used in modern orthodontics, in order to limit undesired side effects of root resorption. For additional information, you can access our chapter on "Neural Modulation of Orthodontic Tooth Movement" in the textbook "Principles in Contemporary Orthodontics". Hope this helps.

http://www.intechopen.com/books/principles-in-contemporary-orthodontics/neural-modulation-of-orthodontic-tooth-movement

Mediators like PGE2 are proinflammatory and any kind of forces whether on compression or tension side will yeild to rise in the level of these mediators. There is no side distinction between compression and tension. However overall bone resorptive ability is dependent on RANK/RANKL/OPG ratio. I suggest you go through the link of systematic review on these mediators below.

dear  Dr Sameera G Nath

: your question  is very  interesting

we have published a Review  paper entitled Molecular Biology of Orthodontic Tooth Movement  with a section entitled Pressure: Tension Related Effects.

here is an abstract which gives you an idea what the paper will discuss in case you decided to read it:

Abstract

The application of orthodontic forces to correct mandibular and maxillary teeth irregularities through alveolar bone remodeling involves

a series of coordinated and regulated molecular and cellular events in the periodontium i.e. periodontal ligament (PL), alveolar bone

(AB), cementum, and gingiva. The PL and AB are the two important structures which actively participate in bone remodeling in response

to mechanical forces. The fibroblasts, osteoblasts, osteocytes, osteoclasts, odontoblasts, cementoblasts, chondrocytes and immune cells

are the major cell types which play an interactive role in the remodeling process. Activation of these cells result in the production of several

pro-inflammatory cytokines, growth factors, colony- stimulating factors, transcription factors and other regulatory molecules which

modulate cell growth, proliferation, migration, differentiation, gene expression and cell function. Recent it has been shown that the role

of SOX 9 gene transcriptase, parathyroid hormone related peptide (PTHrP), Indian hedgehog (IHH) protein in orthodontic tooth movement

orthopaedics is significant in understanding the molecular biology of orthodontic tooth movement orthopaedic forces in growth

modification therapy. In this article, however, we review the major cellular and molecular sequence of events during orthodontic tooth movement, per se.

hope this article helps to answer your very interesting question

sincerly

Prof.Kgalil.DDS.,D.Oral&Maxilliofacial Surg.,Ph.D.,FAGD.,FADI.,Cert .Periodontist

Thank you Galil Sir.

I think that Amit Agrawal's answer responds most specifically to your question. It is a consequence of restricted blood flow on the pressure side only. So that is where the proinflammatory response occurs.