Are Cavitations Real?

At SteinerBio, our posts are accompanied by cited literature to support our discussions. When we are discussing a subject that lacks solid published literature, we make an effort to be clear that we are only providing our opinion. This discussion on cavitations falls somewhere in no man’s land as there is published literature, but little of scientific validity. In dentistry, a “bone cavitation” is a term often used to refer to areas of jawbone that is believed to be lacking mineralization or is very poorly mineralized, and filled with either chronically infected, necrotic (dead tissue), or otherwise pathologically affected tissue. Some practitioners suggest that such cavitations can have systemic health implications and may be linked to various chronic health conditions.

In order to get a generalized opinion of what our profession thinks of cavitations, we consulted A.I. to provide a definition of these two terms as follows:

A.I. definition of a “bone cavitation”:

A bone cavitation in the jaw, often referred to as a “cavitation lesion” or “cavitation,” is a term used in dentistry to describe a specific type of pathological condition that can occur in the jawbone. It is also sometimes called a “jawbone cavitation” or “ischemic osteonecrosis”. Cavitations are not widely recognized or accepted in mainstream dentistry, and their existence and significance are a topic of debate within the dental community.

A.I. definition of NICO:

Neuralgia-Inducing Cavitational Osteonecrosis (NICO) is a controversial and debated term used in some alternative and complementary medicine practices, particularly in the field of dentistry. It refers to a theory that suggests that certain dental cavitations (also called cavitations or dental ischemic osteonecrosis) can cause neuralgia or pain in various parts of the body, including the face and head.

It is obvious that A.I. is as confused as we are regarding these concepts.

Let’s begin the discussion that a cavitation is an area of very poor mineralization in the jaw with no obvious associated etiology. Let’s accept that the area must be filled with abnormal or pathologic tissue to be considered a cavitation, which distinguishes the area from only reduced mineralization.

With these generalizations about how a cavitation can be defined, let’s go to the clinic and evaluate areas in the maxillofacial region that present with these features.

When mandibular cancellous bone is poorly mineralized and provides reduced strength, the cortical and crestal bone reacts by thickening to compensate for the poorly mineralized cancellous bone. In the following case, the mandibular crest is abnormally thickened indicating poor cancellous bone support.


Looking at the bone between the bicuspids, this patient generally presents with normal trabeculae in cancellous bone of good density. However, in the edentulous space, the lack of bone density is obvious, and the thick crest is pathognomonic of a lack of cancellous bone support as identified by the red arrows. The oral clinical appearance of the jaw was otherwise normal. The patient reported no associated pain. A core sample of the tissue was taken at the time of implant placement.

The core sample histologic section displayed minimal mineralized issue.

Histological evaluation shows the area was filled with fat cells. The maxilla and mandible do not contain marrow. The nonmineralized tissue in the maxilla and mandible is called stroma and fat cells are never found in the stroma of normal jaws.

Scattered throughout the fat cells were isolated masses of inflammatory cells which indicate the presence of either pathogens or antigenic debris.

Fat cells are never seen in normal bone in the maxilla and mandible, which establishes this tissue as pathologic.

At the time of biopsy, the clinician knew the cancellous bone was poorly mineralized, but was unaware the tissue was pathologic. The decision was made to stimulate regeneration of the lesion by filling the implant osteotomy with BioDensification and place the implant, which would infuse the tissue with SL Factor in an effort to stimulate regeneration in the compromised tissue.

Three months after the core sample and placement of the implant, the fat filled cancellous bone has regenerated into normal cancellous trabecular architecture with good density and the thickened crest resorbed back into normal crestal bone. After histologic evaluation and recognizing that the tissue was pathologic, a better course of action is to remove the fatty tissue from the lesion, fill the site with graft material such as BioDensification or Socket Graft Injectable, and drive the implant into the grafted bony lesion. These graft materials have been shown to produce integration through the graft material, so a delay in implant placement is not needed.

Osteoblasts are motile regenerative cells with the ability to crawl into the graft material, and when they encounter the implant they produce integration. Fibroblasts and fat cells are motile, but BioDensification, Socket Graft, and Sinus Graft materials were designed to allow for migration of osteoblasts into the graft material while excluding fibroblasts and fat cells. It is this critical feature of selectively allowing bone regenerative cells to enter the graft material while excluding fibroblasts that allows these graft materials to produce integration while no other graft material is capable of this type of performance. In this case, the implant was restored 3 months after core sample and implant placement due to this feature. Integration will not occur with the use of granular graft material. The spaces between the granules do not prevent fibroblasts from entering the graft material resulting in fibrosis on the implant and a failure to integrate.

Most clinicians who place implants have experienced drilling through a hard and dense alveolar crest and falling into tissue that provides no resistance to the drill. Knowing that the implant will be 90% in fatty tissue with no ability to integrate to the implant, the clinician should be prepared to remove the fatty tissue and place a graft material that stimulates bone formation and integration to improve the long term success of the implant.


Tooth #19 was referred for extraction and grafting to be followed by implant placement. However, distal to #19 an area of poor mineralization was detected. The decision was made to extract and graft #19 with Socket Graft Injectable to be followed up with an implant one month after extraction.

During the extraction, a crestal incision was made to the distal of #19 to explore for the possible cause of the poor mineralization. There was no perforation of the crest or the buccal or lingual cortical plates, so an osteotomy was performed on the crest to gain access to the cancellous bone. Upon perforation of the crest, the tissue in the mandible was found to be dark with minimal mineralization and very little bleeding. This tissue was not granulation tissue and gave the appearance of a blood clot. The lesion extended toward the ramus and was easily curetted out resulting in a bony cavity with minimal bleeding. The lesion was grafted with Socket Graft Injectable, and the flaps were closed with 40 Vicryl suture and Oral Bond.

Day of extraction and grafting

Due to the presence of the pathology in area of #18, the decision was made not to perform a one month implant but to do a delayed implant at 3 months.

5 weeks post extraction

At 5 weeks, mineralization in the roots of #19 and in the distal lesion are approaching normal mineralization as seen in the rest of the mandible.

13 weeks post extraction

At three months, mineralization in the grafted areas surpasses the mineralization in the rest of the mandible. The inferior border of the mandible shows significant porosity, which is diagnostic of osteoporosis.

A CT scan of the area of the lesion shows excellent mineralization. The porosity of the cortical bone throughout the mandible is again indicative of osteoporosis. The presence of osteoporosis is not believed to have played a part in the development of this lesion and does not inhibit bone regeneration or long term implant success.

This slice from the CT scan clearly shows the grafted areas have greater mineralization than the surrounding bone.

To understand this complicated lesion, the history of the site was researched. It was found that one year prior, tooth #18 developed a root fracture and was extracted without grafting. The location of the initial lesion on tooth #18 is closely associated to the lesion that was present one year later. One possible explanation for the development of this lesion was proposed by Dr. Charles Ruefenacht. Knowing that when a tooth is extracted and the socket is left exposed to the oral cavity, the bone lining the socket becomes necrotic and is sloughed out of the extraction site over a period of the next 38 days. If those necrotic pieces of bone become trapped in the healing socket rather than expelled, Dr. Ruefenacht proposed that this could produce this type of lesion filled with avascular necrosis.


In the following case, an osteotomy was prepared in the posterior mandible. However, after the hard crest was perforated, the burr fell into the mandible with no resistance. After inspection of the osteotomy, the mandible was hollow containing no tissue. On the floor of the mandible a membrane was found as identified with black arrows:

No cancellous bone

As the mandible was an air-filled cavity, a conservative approach was taken and the anterior area of the mandible was grafted with Socket Graft Injectable limited to the area of the implant as outlined with black arrows below. Due to the consistency of Socket Graft Injectable, the material flows into the empty cavity through the osteotomy allowing for a minimally invasive surgery but bonds to the bone and stays in place as the implant is placed.

Grafted with Socket Graft Putty and implant placement.

2 months post op

Two months post-op the graft material picked up regenerative cells from the floor of the mandible allowing for mineralization to grow into the coronal area and along the implant.

At the healing abutment appointment, the distal portion of the mandible remained hollow. An osteotomy was performed distal to the implant in addition to an osteotomy into the ramus. Socket Graft Injectable was placed into the anterior osteotomy until the graft material was expressed from the osteotomy in the ramus. Again, the consistency of the material allowed for a minimally invasive treatment.

Healing abutment appointment with mandibular grafting.

4 months post graft of mandible

4 months after grafting the mandible, the lesion is now fully mineralized with healthy vital tissue.

These three lesions are presented to document the variety of post extraction lesions found in the jaws. Let’s look at how medicine deals with these terms and lesions.

Avascular necrosis (AVN) is common in the skeleton. It is usually found in the hip and its etiology is associated with long term steroid use, alcohol abuse, or trauma. The lesion begins as an area of dead bone due to a lack of vascular supply and shows radiographically as a hole in the bone. Early researchers did call this hole in the bone a cavitation. When AVN progresses, it becomes painful as the joint collapses. So now we have a hole in the bone that is necrotic and painful. Avascular necrosis is what ended Bo Jackson’s career. In medicine, holes in bone are not uncommon and are an accepted pathology with extensive published research on the subject. However, AVN is not suggested to initiate or aggravate other systemic diseases.

Let’s now transition back to dentistry. While there are significant differences in skeletal and maxillofacial bone, one difference that is obvious is that maxillofacial bone is subject to a much greater degree of pathology. Many people are walking around with such active pathology in their jaws that if this pathology was located in their skeleton, the person would be in the ICU. The maxilla and mandible are unique in their ability to isolate the pathology and limit the spread of the pathology. However, if pathology exists in maxillofacial bones, can we claim that this pathology does not have any potential systemic effects?

Conditions that have been suggested by proponents of cavitations to be related to maxillofacial cavitations include:

  1. Chronic Fatigue Syndrome (CFS)
  2. Fibromyalgia
  3. Autoimmune disorders
  4. Neurological disorders
  5. Immune system dysfunction
  6. Certain chronic pain conditions

Meanwhile, for most of us it is difficult to reason that a localized lesion in the maxillofacial bone can have these systemic effects. In that regard, we should consider the proposed systemic effects of another oral pathology that is limited to the maxillofacial region, such as periodontal disease.

Periodontal disease is known to be associated with several systemic diseases and conditions. While a direct causative relationship may not exist in all cases, there is evidence to suggest that periodontal disease can contribute to the development of or exacerbate certain systemic health issues. Some of the systemic diseases and conditions that have been linked to periodontal disease include:

  1. Cardiovascular Disease: Research has shown a potential link between periodontal disease and an increased risk of heart disease, including conditions like atherosclerosis and heart attacks.
  2. Diabetes: It is proposed that periodontal disease can make it more challenging to control blood sugar levels in individuals with diabetes. Poorly controlled diabetes, in turn, can worsen periodontal disease.
  3. Respiratory Diseases: Periodontal disease may be associated with certain respiratory conditions, including chronic obstructive pulmonary disease (COPD) and pneumonia.
  4. Rheumatoid Arthritis: There is some evidence suggesting a connection between periodontal disease and rheumatoid arthritis, an autoimmune disorder that affects the joints.
  5. Alzheimer’s Disease: While the relationship is still being researched, some studies have suggested an association between periodontal disease and an increased risk of Alzheimer’s disease.

Many in our profession accept the concept of periodontal disease producing adverse systemic effects. If we accept that periodontal disease can have negative systemic effects, how can we intellectually rationalize that cavitations do not have the potential to produce any negative systemic effects?

The three cases presented in this article are all holes in bone. The first two cases are holes in bone filled with pathologic tissue and fit the definition of a cavitation. The third case where bone was filled with air is not filled with pathologic tissue, but therapeutically presents with similar requirements to successfully restore normal mineralization. The first case that was filled with fat and radiographically showed poor mineralization in the body of the mandible and thickened crestal bone are common lesions commonly encountered by implantologists.

Holes in jawbone exist and while these lesions have not been proven to be associated with pain, it is judicious to not rule out the possibility of these lesions producing referred pain, as pain is almost always associated with avascular necrosis lesions in the skeleton.

Regarding these lesions being associated with systemic disease, the link is far less clear, but as science moves closer to understanding how our bodies are interrelated, the concept cannot be ruled out.


If we accept these lesions as real, then we need to begin to understand the etiology of these lesions. The common link with the three cases presented is they all develop following tooth extraction. But more specifically, they only develop when the extraction socket is not properly cared for and treated. In medicine, even the most minor wound is cleaned, closed, and dressed. In dentistry, we continue to create large wounds with tooth extraction and commonly ignore proper care of the wound. We at SteinerBio have never seen a post extraction bony lesion when the socket is cleaned of infection, closed with a biocompatible bone graft, and dressed with a membrane. Tooth extraction without completing the surgery by treating the wound not only causes collapse of the jaw, but also includes potential acute painful infections such as dry sockets. We now must also realize that not properly treating the extraction socket sets the patient up for significant post extraction bony lesions that will be found more frequently when the profession learns how to diagnose these lesions.


Do these lesions need to be treated? The lesions may be quiescent indefinitely, but is it prudent to ignore pathology? Most patients who are informed of the presence of these lesions would prefer to have them removed. In the case of implant placement, it is obvious that all the lesions presented in the article would compromise the success of dental implants. In the three cases presented, the tissue in the areas of these lesions is not capable of integration and could also have the potential of preventing integration. In the case of dental implantology, these lesions need to be diagnosed and treated to restore healthy vital bone for predictable long term implant success. However, it is the treatment of cavitations that has caused so much criticism of those clinicians who treated these lesions in the past. In years past, these lesions were treated by resection, often removing large portions of the patient’s jaw. These lesions are all internal lesions confined to cancellous bone. The crest and cortical bone are never involved with these lesions and should not be removed. In the past, the clinician did not have the regenerative materials and methods to regenerate these lesions. However, we now have the regenerative materials that allow for the lesions to be removed from the jaw followed by the injection of regenerative grafting materials that can restore the affected area to full form and function. At SteinerBio, we are bone biologists who specialize in bone regeneration, but we do not pretend to be bone pathologists. We welcome feedback from those clinicians who have more knowledge and experience in treating these lesions.

Cavitations are real.


American Society for Bone and Mineral Research (ASBMR)

Tissue Engineering and Regenerative Medicine International Society (TERMIS)

American Academy of Implant Dentistry (AAID)