Diagnosis and Treatment of Osteomyelitis of the Jaw – A Systematic Review (2002-2015) of the Literature

Special Article - Oral Health

J Dent & Oral Disord. 2017; 3(4): 1066.

Diagnosis and Treatment of Osteomyelitis of the Jaw – A Systematic Review (2002-2015) of the Literature

Gudmundsson T¹*, Torkov P² and Thygesen TH³

Department of Oral and Maxillofacial Surgery, Odense University Hospital, Denmark, Europe

*Corresponding author: Gudmundsson T, Department of Oral and Maxillofacial Surgery, Odense University Hospital, Denmark, Europe

Received: June 05, 2017; Accepted: June 23, 2017; Published: June 30, 2017

Abstract

Background and Aim: To review the contemporary literature on the various types of osteomyelitis of the jaw and list treatment options, diagnostic measures, opinions and speculations concerning OM of the jaws.

Methods: A Medline (PubMed) search was conducted and articles from 2002 and onwards was chosen.

Conclusion: The current understanding of the predisposing factors and developmental phases of osteomyelitis of the jaw is insufficient. A widely diagnostic consensus is needed if reported data are to be used in meta-analyses.

Keywords: Bone, diagnosis; Imaging, Infection; Jaw; Maxillofacial; Osteomyelitis; Therapy

Introduction

Osteomyelitis (OM is an inflammatory process of the bone. In the maxillofacial skeleton, usually both medullary and cortical bone are involved, hence the term is most often used to describe the inflammatory process in the basal and alveolar bone [1]. The most commonly used definitions of OM are an inflammatory reaction within the bone caused by bacterial invasion [2,3] or merely an inflammatory process of the bone, [4] both cortical and cancellous [5,6]. In the mandible, the most common sites are the body, followed by the symphysis, angle, ascending ramus and condyle [7]. OM is very rarely seen in the maxilla [6].

OM of the jaw can be a difficult disease to treat because the chronic forms have a marked tendency towards recurrence. OM of the jaw is not a singular entity. In the literature, two main types of OM are described. The presence of pus and/or fistulas and/or sequestrations are characteristics of the suppurative variants, thereby distinguishing them from the non-suppurative variants, which are chronic inflammatory processes of unknown etiology [5,6,8]. Even though OM of the jaw is a relatively rare condition, there are numerous differential diagnoses and classifications. Unfortunately, there is a lack of international consensus about their respective definitions, which makes it difficult to analyze and evaluate the reported data. Likewise, there are counter reports of differing treatment plans and find great variation in diagnostic approaches and follow-up regimens. This lack of diagnostic agreement and different approaches to treatment reflects the inadequate understanding of the predisposing factors and processes leading to OM of the jaw.

In the first main type of OM, infectious pathogens can be identified, appearing at different stages in pus, abcess/fistula and sequestration [1]. In the vast majority of these cases, there is an apparent odontogenic, infectious etiology [6] or some level of trauma introducing pathogens into the tissues [5]. This is defined as Secondary Chronic Osteomyelitis (SCO) [5,6,9].

Several authors define this type of OM of the jaw as a condition of inflammation in bone marrow and cortex, with a pathogenesis directly associated with pathogenic microorganisms [1,3,10,11]. Accordingly, this type of OM should be seen only in association with infected foci, or where pathogens have been introduced through the mucous membranes or bony tissue have been exposed. Blood-borne pathogens are also capable of initiating OM of the jaw, which is mostly seen in pediatric patients and in immuno compromized patients [12].

The other main type of OM is a non-suppurative chronic variant with an insidious unexplainable onset, occasionally without culturable/detectable pathogens [6]. This is defined as a chronic inflammatory disorder of the cortical and cancellous bone of unknown etiology [5,8,13,14] or simply as chronic non-suppurative OM [1,6,9]. Characteristic of this type of OM is the lack of an acute state and the development of symptoms over the course of a few days to weeks. There may be periods without symptoms followed by exacerbations [5,8,13]. This definition applies to Primary Chronic OM (PCO) [5,6,9,14], Diffuse Sclerosing OM (DSO) [4], Diffuse Sclerosing OM of the Mandible (DSOM) [4], Juvenile Mandibular Chronic OM (JMCO) [8], Chronic Recurrent Multifocal OM (CRMO) [13], and chronic nonbacterial OM (CNO) [15] In this review these diagnoses are categorized as non-suppurative OM. (The term diffuse sclerotic OM is a broad radiologic description and also an excellent example of the confusing classification of OM. The diagnosis DSO has been reported in both bacterial and non-bacterial OM. Normally DSO is synonymous with PCO) [5,6].

Radiologic, clinical and histologic characteristics mentioned in this selection of articles suggest that these diagnoses describe nearly identical conditions or possibly identical conditions at different expressions or stages. Apparently, the main differentiating feature of CRMO from PCO, DSO, DSOM and CNO is the detection of more than one affected site. Other distinguishing histopathologic features have not yet been established [5,9]. Consequently, PCO, DSO and DSOM are by some considered as expressions of CRMO [4,9]. Eyrich et al. are not convinced as they detected microabscess formation (which is not previously reported in gnathic bone lesions of CRMO and only once in DSO) and no extragnatic involvement in 10 of their 11 childhood and adolescence PCO patients, which seems to suggest a different disease process [5]. Theologie-Lygidakis reports similar finding in three of five juvenile PCO patients [14]. Furthermore, CRMO is considered an expression of the SAPHO syndrome (synovitis, acne, pustolosis, hyperostosis, and osteitis) [4- 6,13]. Several authors agree on this, but according to Bevin et al. there is debate of whether SAPHO syndrome should be recognized at all, as there is less than 50% association of signs and symptoms [9].

PCO seems to have a stage-like course. Initially it is often seen with a radiographically mixed sclerotic and osteolytic pattern, which later on changes to sclerotic [5]. The sclerotic changes are characteristic of DSO.

The term non-suppurative does not exclude the presence of pathogens. It seems unclear whether non-suppurative OM of the jaw is aseptic or not, or if both possibilities exist. Krakowiak et al. describes chronic non-suppurative OM as caused by certain bacteria (Actinomyces and Eikenella corrodens) presenting mild or no symptoms and so often diagnosed several years into the disease process [7]. Other authors report negative bacterial findings indicating a non-bacterial pathogenesis [6,8,14].

Culturing or even detection of pathogens in cases of OM remains challenging. This may be caused by difficulties in biopsy handling and/ or insufficient culturing techniques or it may, in some cases, actually be a result of absence of bacterial pathogens. These hypotheses are not easily validated. Some authors suspect results from biopsies are due to contamination in the trans-oral harvesting procedure [6]. Several scenarios of bias are feasible. It is thinkable that current culturing techniques are predominantly detecting contamination and not the causative pathogens. Maybe the dynamic nature of the flora masks the initiating pathogens as they are later on surpassed by other bacteria. Maybe a polymicrobial flora requires very specific culturing media. Maybe the detected bacteria in non-suppurative OM are due to secondary infection caused by previous surgery or biopsy. Maybe negative culturing is caused by inadequate techniques of biopsy specimen handling or laboratory culturing. Hence it is difficult to conclude if the cultured bacteria are the actual causative pathogens or if negative culturing means that chronic non-suppurative OM of the jaw is aseptic. Only few authors reported negative culturing of biopsies in mandibular OM [6,8,16]. Looking at articles by rheumatologists, aseptic OM of the extremities is acknowledged as a separate entity. CRMO is defined as aseptic [13].

Eyrich et al. suggest an overall OM categorization by defining primary chronic OM (PCO) as a chronic non-suppurative OM of unknown etiology, and secondary chronic OM (SCO) as a condition with suppuration, abscess/fistula formation, and sequestration at a later stage due to a defined, infectious etiology [5].

Another classification is based on duration of the symptoms. Acute OM (AO) and subacute OM are differentiated from Chronic OM (CO) by a time line of (usually) 1 month, meaning that OM is considered chronic if the duration exceeds 4 weeks/1 month [1,5,6,9,14]. Other authors consider OM as chronic when the duration exceeds 6 weeks [17]. This classification is to our knowledge used mainly for pyogenic OM.

OM of the jaw is very likely several multifactorial clinical entities presenting themselves with similar symptoms and radiologic appearances.

Materials and Methods

Selection of articles for this review was made from PubMed searches with the following key words: “Osteomyelitis AND jaw”, “treatment, chronic osteomyelitis AND jaws AND diagnosis”. The focus has been on the contemporary literature; consequently the search was limited to articles published in 2002 and onwards. The titles and abstracts were screened for relevancy. 23 articles were selected for this review. Specific PubMed and other searches in order to find additional material are mentioned in the text. The PRISMA statement was followed [18].

The original intent of this article was a systematic review of the contemporary articles from 2002 and onward. The aim was to categorize reported diagnostic and treatment modalities for the infectious and non-suppurative types of OM of the jaw and statistically evaluate the clinical outcomes in terms of success rates, failure rates and expected rates of recurrences. However, this turned out nearly impossible, as the lack of international diagnostic agreement and differing diagnostic measures were encountered. Due to the rarity of some forms of OM, articles are often presenting a very modest number of patients without control groups, making the level of evidence low. Consequently, it was decided to review the contemporary literature and list treatments, diagnostic measures, opinions and speculations concerning OM of the jaws.

Diagnosis

OM of the jaw has proved a challenging condition to effectively diagnose, treat, and cure. As previously mentioned, there are multiple diagnoses for different manifestations of OM of the jaw, some of which are sub classifications, other may be the same condition in a different stage or a different expression. Some diagnoses merely reflect the radiologic appearance, the number of affected foci, the age group of the patient, the presence or absence of pus or recurrent nature of the disease. Many different diagnostic techniques have been proven to be useful, but so far the agreement among many authors is that the final diagnosis should be based on the following parameters: (1) the clinical presentation and history of the patient, (2) imaging techniques,(3) culturing, and (4) histologic analysis [12,14].

Clinical presentation

Local intense pain, tenderness, fever, painful or painless swelling, purulent discharge, intraoral fistula, skin fistula, trismus, hypoesthesia of the inferior dental nerve, and pathologic fracture are among the common symptoms in suppurative OM. If the bacterial infection is less virulent, symptoms can mimic an acute or prolonged alveolar osteitis making diagnosis and selection of relevant treatment difficult [1].

Non-suppurative OM of the jaw, e.g. PCO, is characterized by recurrent pain, swelling, limited mouth opening, absence of suppuration [8,9], periostitis, occasionally regional lymphadenopathy and reduced inferior alveolar sensation [6].

Radiographic appearance

PCO in the mandible is typically seen with a mixed pattern of sclerosis and osteolysis [5,14]. There may be widening of the mandible, periosteal bone reaction [8,13] and an unidentifiable cortical-medullary border [5,6]. In the later stages there seems to be a shift towards only sclerotic changes [5,6]. Lamination of periostal new bone and sequestra are radiologically distinguishing features of OM [10]. PCO often show patchy osteosclerosis and osteolysis and frequently the “onion-skin appearance” of subperiostal bone formation [9].