The exact mechanism of osteonecrosis depends primarily on the predisposing cause. This is reflected in the table below. Osteonecrosis is generally thought of being an irreversible process. If the necrosis occurs next to a joint surface, it is generally considered to cause joint deformity.
However, no one really knows if this is true, and such conclusions are to some extent artifacts of our current diagnostic methods for osteonecrosis. With the advent of MRI, we finally have a tool which can show abnormalities within about 2 weeks of the original insult. However, current standard MR scanning cannot yet show abnormalities at the instant of infarction.
What is needed to answer this question is a diagnostic technique that is sensitive to vascular flow, and not just intensity changes in the bone marrow.
Dynamic MR scanning following a gadolinium bolus may be helpful in this regard, but definitive studies have not yet been done to prove this speculation. There is some evidence in the literature that suggests that in some circumstances, osteonecrosis may be a reversible process that can resolve completely without subchondral collapse and subsequent joint arthrosis.
This evidence is found in the literature for transient osteoporosis of the hip, an idiopathic disorder characterized by a reversible osteopenia of the hip and marked marrow edema.
These biopsies have shown the presence of osteonecrosis in many cases, leading to the suggestion that TOH may actually be due to a low-grade and reversible osteonecrosis. It turns out that, in part, the shape of joints governs the distribution of osteonecrosis. In particular, it is the convex versus concave shape of the opposing joint surfaces of most joints that determines this distribution Simkin et al.
On both sides of the joint, the forces of weight-bearing and other loading are directed tangential to the joint surface. On the convex side of the joint, these forces converge to a common center. On the concave side, these forces diverge away from each other. To see the significance of this fact, one must first consider the phenomenon of hydraulic resistance.
One can think of the bones as calcium balloons filled with water. Water is not compressible, so this internal water provides some support to the bones, and this supporting force is called hydraulic resistance. Nature is thrifty, and the presence of hydraulic resistance makes it possible to provide the same support with less bone.
Since the loading forces converge to a common center on the convex side of the joint, hydraulic resistance becomes a fairly efficient mechanism for resisting these forces. On the concave side of the joint, the divergent nature of the forces makes this mechanism much less efficient, and therefore, hydraulic resistance plays a much smaller role in bone support. The two sides of the bone are obviously supporting the same load, so more bone is therefore necessary on the concave side.
All bones of the skeleton are affected. Relative ease of bone exposure after extraction of a tooth contributes to the development of bone infection and necrosis. Due to a generalized involvement, this condition can also be called osteochemonecrosis. The bisphosphonate medications tend to selectively target and destroy osteoclasts, altering the bone metabolism and allowing a unilateral osteoblast-mediated bone build-up.
This results in a formation of dense and poorly vascularized bone. Due to the involvement of the entire jaw, BRONJ cases tend to be treated more conservatively than cases of osteomyelitis or osteoradionecrosis, where surgical debridement is important.
Both CO and BRONJ can have similar signs and symptoms, are most commonly found in the posterior mandible, and result in the formation of necrotic bone in the jaws.
Although there is no data on the interplay of multiple factors in these conditions, immunocompromised patients on long-term treatment with NBPs, who concurrently have an advanced dental disease, need to be evaluated for CO so an accurate diagnosis can be established and a targeted treatment plan implemented. In this report, the authors describe a challenging case involving a patient who developed jawbone necrosis. It emphasizes the importance of a proper differential diagnosis—including BRONJ and CO—while accurately determining the final diagnosis so that the proper therapy can be instituted.
The authors followed the guidelines of the Helsinki Declaration for this study. This article was exempt from the institutional review board approval. In addition, the patient had hypertension, right total hip replacement surgery without complications 3 years prior, and was allergic to penicillin. On examination, the patient had a decayed remaining lower right third molar root with associated mild swelling and erythema of the surrounding tissue.
A panoramic radiograph showed a small portion of the third molar root mainly in the soft tissue above the alveolar bone level Figure 1. The day after presentation, the patient underwent extraction of the root of the lower right third molar without complications.
One hour prior to her surgery, the patient took mg of clindamycin, and she continued on mg of clindamycin three times daily for the next 5 days. The patient returned for follow-up examination 1 week postoperatively and demonstrated normal healing for this timeframe.
One month later, the patient called to report swelling and pain in the area of the extraction site. On examination, swelling was evident in the posterior mandible in the area of extraction, extending to the buccal vestibule and masseteric region, with limited mouth opening to about 15 mm, and purulent discharge behind the second molar.
Given that this condition had existed for 6 to 8 weeks, the preliminary diagnosis of CO was made, and the patient consented to indicated treatment, which consisted of debridement of the wound and extraction of the second molar. The procedure was performed on the same day under local anesthesia; mg of clindamycin was given just prior to the surgery.
A buccal full-thickness flap in the second-third molar area was raised, and multiple small bony sequestra with granulations tissue were visualized and removed until fresh bleeding bone was seen; the involved second molar was also removed with copious irrigation after debridement.
The patient was placed on clindamycin mg four times daily and was followed weekly. Four weeks later, the wound remained open with purulent discharge. A second, wider bone debridement procedure was performed, with removal of a few more necrotic bone fragments. The agreed upon approach was to discontinue the alendronate and to decrease the dosage of prednisone from There was a temporary improvement in her jaw symptoms, but after 5 to 7 days, infection with purulent discharge returned.
Follow-up imaging, including a panoramic radiograph Figure 3 , showed persistent mottled, mixed irregular radiolucent-radiopaque appearance, slightly more extensive than that seen on the previous panoramic image. The third debridement of the wound was performed 10 weeks after extraction of the root of the third molar, which was 6 weeks after the first debridement and 3.
A large amount of granulation tissue and multiple sequestra of devitalized bone were curetted out down to vital-appearing bleeding bone. A second culture and sensitivity test did not reveal the presence of microorganisms. Because of concerns for mandibular osteomyelitis and possibly actinomycosis , the ID physician discontinued oral clindamycin, and the patient was placed on a 6-week course of intravenous ceftriaxone 2 gm, once a day through the peripherally inserted central catheter PICC line.
In 48 to 72 hours, the patient reported much improvement in symptoms. Granulation tissue began to fill the wound, negating the need for further debridement.
After 6 weeks of ceftriaxone, complete closure of the wound was occurring, and a panoramic radiograph demonstrated significant remodeling of the bone without a mottled appearance or evidence of sequestration. Although the patient subsequently developed diabetes mellitus DM type 2 and was placed on insulin, it did not complicate the wound healing Figure 5.
Upon discontinuation of ceftriaxone, the ID physician returned the patient back to a 3-week course of oral clindamycin mg, three times a day. The last panoramic radiograph taken on this patient was 5 months after the initial presentation and 3 months after the last debridement.
It demonstrated partial fill of the mandibular defect and bone remodeling without evidence of necrosis Figure 6. A few oral conditions can present as non-vital necrotic bone in the jaws, including: chronic suppurative osteomyelitis CO , osteoradionecrosis, osteopetrosis, and bisphosphonate-related osteonecrosis of the jaws BRONJ.
Although any of these processes can develop in the immunocompetent individual, they can initiate much earlier and progress much more quickly in an immunocompromised patient or one with autoimmune disease on immunosuppressive medications, such as the patient in the described case report. The patient in this case report had RA—a systemic chronic inflammatory autoimmune disease that usually occurs in middle-aged women and affects mainly joints and other tissues and organs lungs, pericardium, sclera, etc.
No statistically significant differences were found between groups for any parameter. Necrotic bone was common to all three diagnoses. Inflammation and reactive bone formation were present in all three diagnoses. The presence of bacteria was a prominent feature in all cases.
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