Killing Regeneration and
Extraction Socket Pain

Bone cells live in the most protected environment in the body. Bone cells are encased in thick cortical bone that is never exposed to the surrounding environment. Bone cells are protected from thermal shocks, physical trauma, pressure gradients, and are bathed in very closely controlled conditions of pH, salinity, hydration, and nutrients. If this protected environment is breached, the regenerative cells that we work with are easily killed. In a previous article, we talked about the importance of biocompatibility for bone regeneration. We discussed the requirement that for healthy tissue to grow, it must do so in an inflammatory-free environment. Today we will discuss how dentists routinely compromise the health of bone and how to avoid killing regeneration.

We will use socket grafting as an example of what is good and what is bad for bone regeneration.

First, we need to understand that the bone in the socket is not infected. While there are theories about residual quiescent bacteria present in bone, they remain theories and here at SteinerBio, we have never seen histology to support these theories. A tooth is often extracted because it is a nidus of infection and when removed, the infection can be effectively treated. After the tooth is removed, the granulation tissue is likewise infected and needs to be removed. After granulation tissue is removed, the entire infection is now removed. In the presence of infection, the body mounts an inflammatory response. It is this inflammatory response that triggers bone resorption, not the infection.

Bone is resorbed ahead of bacteria. However, there are very rare instances that bacteria reaches the bone, causing osteomyelitis, which is a surprisingly rare occurrence in the jaws. The bone that is exposed after tooth and granulation removal was not infected prior to extraction, but surely after vigorous removal of granulation tissue, the surface bone will become contaminated with bacteria. You have never seen a bacterial plaque on bone in an extraction socket. The bacteria are not colonized and are merely scattered over the surface as a result of debridement. For this reason, it has been shown that simple rinsing of the socket with sterile saline reduces residual bacteria by 60%. The reason a simple rinse is effective is because the bacteria are scattered over the surface and are not present in attached organized colonies. If you want to grow normal healthy bone, the bone should not be tampered with after tooth and granulation tissue removal, nor should medications or antiseptics ever be introduced into the socket other than a gentle sterile saline rinse. This is not taught by professors and lecturers who usually only have experience with cadaver bone grafts and have no experience regenerating normal healthy bone with science-based bone grafts.

Professors and lecturers who only use cadaver bone grafts commonly teach aggressive post-extraction debridement, often combined with the application of local antimicrobial treatment because of the potential of infection of cadaver bone grafts. Not only is infection of cadaver bone graft common, but infection of cadaver grafts can go unnoticed. After a socket has been filled with mineralized cadaver material, the only thing that is seen on a radiograph is the dead bone of the graft that blends in with the existing bone. You cannot see if mineralization is occurring or if infection is present. The following case is an example.

The Application

When bone is injured, the first phase of healing is a fibrin clot. The fibrin clot is composed of fibrin, red blood cells and acute inflammatory cells.
The left radiograph is of #7 and the right radiograph is #8. Both sockets give a normal radiographic appearance as the cadaver bone graft blends in with the surrounding bone. Since the sockets are filled with dead bone, it is not possible to determine if mineralization is occurring or if infection is present.
At 7 weeks, socket #7 is healing normally with intense inflammation to the graft material and incipient mineralization on the allograft particles.
Socket #8 likewise shows the normal inflammatory infiltrate to the cadaver graft particles, however, no mineralization if found.
Upon histologic inspection, the socket of #8 is infected. There is no purulence, swelling, or gingival inflammation because this bacterium has coated its colonies with host antibodies to hide from the host immune system.
Cadaver bone grafts all have a very porous structure that makes the particles ideal for bacteria to colonize in an isolated environment, protected from both antibiotics and the host immune system.

Because of the propensity of cadaver bone grafts to become infected, dentists have developed aggressive decontamination methods to prevent cadaver bone graft infections. While there is no standardized method of post-extraction decontamination, most lecturers will have their own preferences for treating the extraction socket.

Due to the potential for infection, many clinicians who use cadaver bone grafts will choose to not graft an infected extraction socket at the time of extraction, but wait until the socket has time to resolve the infection prior to grafting. These clinicians are primarily those who are limited to the use of cadaver bone grafts and do not avail themselves to science-based grafts that are bacterially resistant. There is no reason for subjecting a patient to a second surgery to graft an infected socket. SteinerBio’s science-based bone grafts are bacterially resistant because our graft materials cannot be the nidus of an infection. By design, both SteinerBio granules and putties cannot be colonized by bacteria. The pore size on our βTCP granules is too small for bacterial colonization and our putties resist bacteria because bacteria cannot migrate into the graft.

A routine procedure after extraction is to use burs to remove granulation tissue and to perforate the socket wall to induce bleeding. However, any cutting, grinding, or scraping of bone kills the remaining cells to a depth on the remaining surface of bone. This fact is evidenced by the knowledge that after implant placement, the stability of the implant drops in the early weeks after implant placement. This decrease in stability is because the drilling of bone kills the cells on the surface of bone adjacent to the implant. Therefore, this bone then needs to be removed by osteoclastic resorption before osteoblasts can migrate to the implant and begin the integration process, thus resulting a decrease in implant stability. Dentists are taught that you must create bleeding in the socket to facilitate mineralization, but again, this is only when cadaver bone grafts are used. Vascular supply is necessary for cadaver bone graft mineralization to occur because cadaver bone grafts mineralize as a result of the inflammatory response to the foreign proteins in the cadaver graft and it is the vascular supply that transports the inflammatory cells.

The inflammation produced by the cadaver bone grafts uncouples normal bone formation where osteoblasts and osteoclasts work in unison to grow and remodel bone. This uncoupling of bone formation and resorption favors mineralization, but the bone that is produced is sclerotic and once formed, it never remodels.

The only way sclerotic bone remodels back into normal bone is when the source of inflammation is removed. In condensing osteitis, the sclerotic bone is present as long as the dental pulp is inflamed. If the pulp is removed, the sclerotic bone remodels back into normal bone. However, the source of sclerotic bone is never removed when an articular joint becomes sclerotic because the osteoarthritis is never resolved. Likewise, when cadaver bone grafts are placed, much of the cadaver bone graft remains in the site so that the sclerotic bone never converts back into normal bone.

So again, the grinding and drilling of the socket wall produces a surface of necrotic bone that is made to prevent post-operative infection and to supply blood that brings in cells of the immune system to produce mineralization when using cadaver bone grafts. None of this is necessary for science-based based bone grafts, and doing so kills the surface regenerative cells and fills the grafted site with blood that significantly delays normal bone formation.

Bone growing cells are never found in blood, blood clots, or healing granulation tissue. In order to prevent the delay of bone formation, blood, blood clots, and healing granulation tissue must be avoided. Some lecturers claim that the periodontal ligament (PDL) needs to be removed and also advise to scrape the socket wall to remove any remnants of the PDL. There is no scientific support for removing the PDL and by doing so, it only injures the socket wall, again, delaying bone formation.

After physically drilling, grinding, and scarping the socket wall, many professors and lectures advise applying antimicrobial therapy to kill residual bacteria. For example, the clinically used concentration of CHX (2%) permanently halts cell migration and significantly reduces survival of fibroblasts, myoblasts, and osteoblasts.

Low pH solutions decrease cell viability and induce cell death in osteoblasts. Viability of osteoblastic cell line, MC3T3-E1, was markedly influenced by the acidity of the culture media in which they are grown. Both pH values of 6.4 and 6.8 induced a significant decrease in cell viability compared with that of pH 7.4 (P < 0.05). Meanwhile, all cells died when cultured in media at pH 6.0.

The pH of betadine is 4.2. Applying betadine to bone will cause significant cell death.

A common antimicrobial for an infected socket is powdered tetracycline. The pH of 1% tetracycline is 2.0. A powdered solution of tetracycline will have an even lower pH and will be toxic to any bone cells. In addition, tetracycline makes no sense as a one-time antimicrobial because it does not kill the bacteria, but stops replication. Stopping replication of the bacteria will not be effective as a one-time application. The only possible benefit of applying a concentrated solution of tetracycline is that it is so toxic with the low pH that it will kill bacteria at the same time it kills all the surrounding bone cells.

Gentamycin is another common antibiotic recommended for socket application. Gentamicin is a clear, colorless solution, having pH ranging from 3.0 to 5.5. At this pH, it is obviously toxic to bone cells.

If the clinician feels compelled to apply an antibiotic to bone, they should use an antibiotic that is made for IM or IV use. These solutions are buffered and avoid the low pH of most of these medications.

Laser application to the bone of an extraction socket is a common recommendation. If the laser is set to a level of intensity designed to stimulate bone formation, it will not be intense enough to kill bacteria. If the laser is set to an intensity designed to kill bacteria, it will also kill bone cells.

So, drilling and grinding bone kills surface bone cells and the application of toxic medications can penetrate to kill an even deeper layer of bone cells. This therapy is advised for cadaver bone grafts because it is effective in killing bacteria and preventing infection. In addition, it does not significantly slow the mineralization process because with cadaver bone grafts, the mineralization process is dependent upon the inflammatory response and is not limited to the production of bone by way of migrating osteoblasts.

What is advised for cadaver bone does not translate to science-based bone grafts. Science-based bone grafts require an inflammation-free environment for bone formation. In addition, science-based bone grafts relay only on viable osteoblasts and their progenitors to form bone. The treatment advised for cadaver bone graft sockets kills off these cells and the area of damaged bone then needs to be removed by osteoclasts before bone formation can occur. The scenario is the same for implant integration. The drilling of bone damages the surface bone cells that now need to be removed before integration can begin. Simple drilling for implants only kills the very surface cells, but when you drill and scrape aggressively and then apply chemicals that penetrate and kill cells to a certain depth, a great deal of resorption, remodeling, and regeneration needs to occur in the damaged bone before bone regeneration can occur in the grafted socket.

With this knowledge we can now move on to the subject of this post. When using cadaver bone grafts, aggressive socket treatment does not interfere with mineralization and prevents bone graft infections, but aggressive socket treatment produces bone graft failure and produces delayed post extraction pain when using SteinerBio science-based bone grafts.

Let’s look at a few cases to understand this concept.

This is an extraction site 6 months post-op on a healthy young woman. The area of sclerosis is defined by a radiolucent border outlined by the blue arrows. The area of sclerosis cannot be caused by the presence of cadaver bone because the area of sclerosis is much larger and outside the confines of the socket that was filled with cadaver bone. This rounded ball shaped area of sclerotic bone is very common, but only found with cadaver bone grafts.

So what can cause this common finding?

It is not logical to think the cadaver bone can migrate into the surrounding tissue, but it is logical that the presence of the cadaver bone graft can prevent the surrounding bone from healing normally. Most clinicians aggressively treat the socket after extraction and grafting with cadaver bone. This kills the surrounding bone. The socket is then filled with a cadaver bone graft that produces sclerotic bone. The cells that produce sclerotic bone secrete osteogenic molecules that increase mineralization and also secrete molecules that stop osteoclast formation. This is the process that produces the dense sclerotic bone seen in the radiograph.

It is reasonable to assume these molecules migrate out of the extraction socket into the surrounding bone and likewise increase mineralization and stops resorption, resulting in the ball of sclerotic bone found in and around sockets grafted with cadaver bone grafts. Every dentist who places implants recognizes this bone as being hard with minimal or no bleeding and drills like chalk. In this bone, you will never find any osteoclasts and therefore, the bone never remodels into normal bone. The inflammatory allograft particles persist indefinitely, making the bone indefinitely sclerotic.

Now let’s see what happens when using SteinerBio’s science-based bone grafts:

This radiograph is two weeks after extraction and grafted with Socket Graft. You can see that 2/3 of the socket is filled with visible mineralization.

Four weeks after extraction, the mineralization has reached the crest. Unlike cadaver bone grafts where all of the early radiopacity is from dead bone, all of the radiopacity shown in these radiographs is from newly formed rapidly growing bone. In these cases, the extractions were all atraumatic by sectioning of the teeth. After tooth removal, all granulation tissue is removed with localized hand instruments and then the sockets are rinsed twice with sterile saline and nothing else.

In this case, if you extracted the tooth, drilled and ground the socket, and then soaked with a toxic antiseptic or applied laser therapy to kill bacteria, you would have killed all of the surrounding bone in the socket and none of this bone formation would have occurred in this time frame.

To utilize the advantages of a science-based bone graft like Socket Graft, you must have immediate osteoblast migration into the graft material. How can this happen if you have just killed all of the osteoblasts in the surface of the bone? When you kill the osteoblasts on the surface of the bone, how can your bone graft become successful when there are no cells to turn the graft material into bone? The killing of the surface osteoblasts is the largest reason for bone graft failures when using science-based bone grafts.

Let’s compare. Cadaver bone grafts heal through an inflammatory process and not from normal migrating osteoblasts. Killing the osteoblasts by aggressive treatment of the socket does not impair the production of mineralized sclerotic bone, but does stop the normal bone formation when using science-based bone grafts. The presence of cadaver bone induces mineralization, but also blocks resorption by preventing the formation of osteoclasts.

So far, we have discussed how the aggressive treatment of the extraction sockets facilitates sclerotic mineralization of cadaver bone grafts and blocks normal bone formation using science-based bone grafts. However, there is one crucial factor that we have not discussed because we needed to provide you with the physiology of the healing socket so that you can understand this next concept.

When you aggressively treat an extraction socket and kill the surrounding bone and then graft with a cadaver bone graft, post operative pain gradually fades. However, when you aggressively treat an extraction socket and graft with a science-based bone graft material, it is not uncommon to experience and increase in post-op pain a few days after extraction. Now that you have an in-depth understanding of what is happing in the socket, we can explain why this happens.

Osteoclasts are responsible for the stimulation and growth of sensory nerve fibers in bone. This makes very good sense because osteoclasts are responsible for removing damaged bone and remodeling bone into normal functioning bone. Wherever osteoclasts migrate to, sensory nerve innervation follows. Nerve innervation is required for normal bone to grow and adapt. In sclerotic bone produced by cadaver bone grafts, you have no osteoclasts present in the newly formed bone and therefore when you kill the bone with aggressive socket treatment, the patient does not experience post operative pain because there are no sensory nerves to feel the pain.

However, when bone is killed with aggressive socket treatment and a science-based bone graft is used, osteoclasts become very active in attacking the damaged bone and bring along sensory innervation. The presence of osteoclasts and the sensory nerves that they bring into the site is what is responsible for the delayed post operative pain when bone is damaged with aggressive socket treatment.

Clinicians only get training from lectures who use cadaver bone grafts and when they substitute a science-based bone grafts for a cadaver bone grafts, they often will produce poor bone graft results with post operative pain.

When we speak to clinicians about socket grafting complications with our products, the response is always the same. They are following the advice of prominent lectures who lack the knowledge about using science-based bone grafts and the techniques they recommend kill regeneration and induce post operative pain.

Our website has a simple list of do’s and don’ts when using science-based bone grafts. Science-based bone grafts are a new world for most clinicians, but by following a few simple rules makes it possible for a successful transition from old technology to the new field of regenerative medicine.

Our profession does not have a solid understanding of dry sockets (alveolar osteitis). It is hopeful that those interested in this subject can use the information presented here to better understand the symptoms associated with alveolar osteitis.


American Society for Bone and Mineral Research (ASBMR)

Tissue Engineering and Regenerative Medicine International Society (TERMIS)