INFECTIOUS AND NONINFECTIOUS INFLAMMATORY DISORDERS: REACTIVE BONY CHANGES, OSTEITIS, OSTEONECROSIS, AND OSTEOMYELITIS
- Bony reactions and erosive changes are common to many different pathologic processes and sometimes critical to accurate diagnosis and medical decision making.
- Bone findings are best evaluated by computed tomography, but magnetic resonance and radionuclide studies are useful adjuncts in selected circumstances.
- Limitations of magnetic resonance imaging must be understood when bone findings are in the critical decision pathway.
Bone involvement is often a critical factor in the diagnosis and treatment planning of inflammatory, neoplastic, and other head and neck lesions. The bone may be the primary site of an inflammatory lesion, be secondarily involved, or be merely reacting to adjacent pathology in a manner that is not important in medical decisions. The bony pattern of involvement also serves as a general timetable of the pathologic process as well as a measure of the potential for aggressive behavior. These changes are best appreciated on computed tomography (CT) and plain films (Fig. 14.1) but can be noted on magnetic resonance imaging (MRI) (Fig. 14.2) and in some cases, such as marrow space processes, are better appreciated with regard to their extent on MRI. Reactive bony changes tend to have a nonspecific appearance of variable increased tracer activity on radionuclide studies, but some differentiation is possible, given the appropriate clinical setting, with a combination of bone and gallium scanning (Fig. 14.3). Ultrasound has no value in evaluating such changes.
A chronic inflammatory mucosal origin process often produces sclerosis and thickening of the adjacent bone. Such a sclerotic reaction is probably most frequently present in the maxillary and sphenoid sinuses of patients with chronic recurrent or persistent sinusitis.1 It occurs in many circumstances, and this bony response is often called reactive osteitis (Fig. 14.4) or osteoneogenesis, but the bone reaction should not be confused with bone infection.2 The reactive new bone is only the result of chronic adjacent inflammation and/or infection and not actual infection of the bone.
Thickening and sclerosis of bone in this setting is the result of slow, appositional growth of periosteal new bone (Fig. 14.4); if the process inciting the reaction is extensive and long-standing, it can become quite thick and obliterate a sinus lumen entirely. Occasionally, its appearance is useful in differential diagnosis. Reactive-appearing bone can also fill the cavity of bone lesions, and its appearance can mimic a matrix-producing process.
If the involved bone is trabecular, the trabeculae may become individually thickened and there will be concomitant crowding out of marrow in the spaces between the trabeculae, usually by a combination of reactive bone and fibroproliferative change (Fig. 14.5). This is seen in both the membranous and enchondral bones of the face and skull and in the ossified parts of the laryngeal skeleton as a reaction to inflammatory or neoplastic disease (Figs. 14.2, 2.14, and 4.14). Such changes are common in the mandible, where they are ubiquitous as areas of “condensing osteitis” in the marrow space surrounding the roots of teeth suffering from chronic periodontal and endodontal infections (Fig. 14.7) and in the mastoid air cells as the result of a long ago resolved chronic mastoiditis (Fig. 14.8).3 It is seen less commonly as an end-stage reactive change at other sites, such as the inner ear suffering obliterative labyrinthitis due to prior meningitis (Fig. 14.9).
Such bony changes can also be due to metabolic bone disease or other systemic diseases (Fig. 14.10) and should be recognized as such if the changes are more generalized than localized in the skull and/or face (Fig. 14.11).
The appearance and evolution of bone infections or inflammation will depend on the virulence of the inciting factor, host factors, blood supply, and treatment history.
Acute, Subacute, and Chronic Osteomyelitis
Both acute and chronic osteomyelitis are essentially always bordered by soft tissue swelling.1,4 The typical inflammatory morphology of this soft tissue reaction is discussed in conjunction with the basic pathophysiology and pathoanatomic correlates of infection and inflammation as seen on imaging studies in Chapter 13. In acute suppurative infections, there will very often be an associated subperiosteal or more extensive fluid collection (Fig. 14.12). More chronic soft tissue reactive changes, such as those seen with skull base osteomyelitis, usually are less edematous in overall morphology and cannot be distinguished from infiltration of the adjacent soft tissues by “small round cell neoplasms” such as leukemia, lymphoma, and plasmacytoma or chronic immune-mediated processes such as sarcoidosis (Chapter 18), Wegener granulomatosis (Chapter 17), and Langerhans histiocytosis (Chapter 19),2 all discussed and illustrated subsequently in the indicated chapters dedicated to these specific diseases. Such changes in bone due to matrix-producing tumors (Chapter 12), metastases (Chapter 42), and primary nasopharyngeal carcinoma (Chapter 188) can also mimic or be mimicked by infection (Fig. 14.13). Such chronic skull base infections are more likely to be fungal or due to more indolent organisms such as actinomycosis.