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Suppurative osteomyelitis

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Author: Sanketh DS, MDS


Osteomyelitis refers to the inflammation of the medullary portion or the marrow space of the bone. The term is derived from Greek words “osteon” (bone) and “meulinos” (marrow). But in a broader sense osteomyelitis is used to describe an inflammatory process affecting the marrow and extending to the cortex as well as the periosteum of the bone.

Suppurative osteomyelitis of the jaw is a condition when an inflammatory process in the medullary portion of the bone leads to edema and pus accumulation in the marrow spaces. Accumulation of purulent exudate builds up medullary pressure and obstructs the local blood supply leading to necrosis of the bone.  


There are many different types of osteomyelitis. In fact, several classification systems have been proposed to group these conditions which have unfortunately resulted in confusion.

Broadly, there are osteomyelitis lesions causing suppuration and those not causing suppuration.

Suppurative osteomyelitis has an acute and a chronic form. This disease is characterised by formation of pus, fistulae and sequestrum (or dead/necrotic bone).
Non-suppurative osteomyelitis on the other hand comprises a group of chronic conditions where there is no suppuration or formation of fistula. This group includes chronic focal sclerosing osteomyelitis, chronic diffuse sclerosing osteomyelitis and chronic osteomyelitis with proliferative periostitis also called Garre’s osteomyelitis.

There is another classification called the Zurich system,

which employs a simple classification categorising osteomyelitis as acute, primary chronic and secondary chronic osteomyelitis. Acute and secondary chronic osteomyelitis refer to the acute and chronic suppurative forms of osteomyelitis respectively. The primary chronic osteomyelitis is used synonymously with chronic diffuse sclerosing osteomyelitis. The synonymous usage of these terms is common in German and continental European medical and dental literature.


Lets’ just quickly go through the gross histology of bone so that we could better understand the pathophysiology behind suppurative osteomyelitis. Most bones like the mandible for example, have a rigid outer compact bone or cortex forming an outer shell surrounding a medullary cavity or marrow cavity. The outside of the compact bone is lined by periosteum. The medullary cavity comprises of medullary or cancellous bone comprising numerous interconnected bony trabeculae. Apart from the trabecular or cancellous bone, medullary cavity also harbours bone marrow and blood vessels. The bulk of the cortical bone is made of concentric lamellae. Concentric lamellae make up the basic metabolic unit of bone and are called osteons or haversian systems. These haversion systems have cylindrical canals called haversian canals housing blood vessels and nerves. These haversian canals communicate with each other as well as the periosteum and the marrow space via canals called Volkmann canals. Volkmann canals like haversion canals also contain blood vessels. This system of interconnected haversian and Volkmann canals, supplies nutrients and nourishes the bone.


Acute and chronic suppurative osteomyelitis are the same disease in different stages of their course. They are separated by an arbitrary time limit of one month. Hence an acute suppurative osteomyelitis that continues its course without subsiding beyond an arbitrary time limit of more than 4 weeks is considered to be chronic suppurative osteomyelitis.  

Suppurative osteomyelitis strictly speaking is a true infection of the bone caused by pyogenic micro-organisms. It is a polymicrobial disease with Staphylococcus aureus, S.albus and S.epidermidis being the major pathogens. Anaerobes like Prevotella, Bacteriodes and Porphyromonas have also been cultured from the diseased site.

However, other factors like radiation and traumatic injuries like gunshot wounds, traumatic tooth extractions and surgeries could also cause the disease. Apart from these factors there are several systemic and local conditions that could alter vascularity of bone predisposing it to suppurative osteomyelitis.

Suppurative osteomyelitis of the jaw is primarily caused by infections usually from infected teeth or periodontium. There is a delicate balance maintained between the micro-organisms and the host immune system. Otherwise every tooth infection or periodontal disease could result in osteomyelitis. Factors favouring microorganisms are their number and their virulence. Factors in favour of the host are host immunity and local blood supply to tissues. Anything that could cause an increase in number and virulence of microorganisms or a decrease in host immunity and local blood supply could result in infections causing suppurative osteomyelitis.  

Micro-organisms elicit an inflammatory response and can locally cause an increased vascular permeability leading to accumulation of plasma fluids. Leukocytes are recruited to the site of inflammation and release numerous proteolytic enzymes that cause tissue damage and necrosis. Inflammatory responses also induce thrombus formation in blood vessels causing ischemia and necrosis. As plasma fluids and pus accumulate in the medullary cavity, they increase the medullary pressure causing vascular collapse of vessels and help in progression of ischemia and necrosis in the marrow cavity.

The pus accumulating inside the medullary cavity could also compress the inferior alveolar nerve causing paraesthesia. This is called as Vincent’s symptom.

Further, pus moves through the medullary spaces and reaches the cortex. Here the pus starts to trickle in through Volkmann canals and haversian systems to accumulate below the periosteum. This compromises the periosteal blood supply. This may further cause lifting and perforation of the periosteum causing pus to accumulate under the mucosa leading to fistula formation and drainage of pus in the oral cavity.  When bone fragments die due to ischemia, these fragments are separated from the normal bone by osteoclastic activity. These separated necrotic fragments of bone are called sequestra.   


Suppurative osteomyelitis can occur in both males and females at any age. Mandible is more often affected than maxilla. This is because maxilla has a rich blood supply as compared to mandible. For the mandible its major source of supply is the inferior alveolar artery. Also since maxilla has thinner cortical plates and lesser medullary bone, infections readily diffuse into the soft tissues and sinuses. Patients with the acute form of the disease may have intense pain, swelling of the jaw, trismus and a rise in temperature (fever). There may be pus exuding out through the gingival sulcus. Patients may have paraesthesia of lower lip (Vincent’s symptom) due to compression of the inferior alveolar nerve. The symptoms in the chronic form of the disease are milder with pain and swelling being less severe. The chronic disease is characterized by formation of fistula and sequestra formation. Fistula could be on the gingiva or even cutaneous with pus exuding out through the skin.


Radiographs of individuals with acute suppurative osteomyelitis do not show changes readily. Rather it takes at least 2 weeks for changes to be noticeable in the radiograph. The acute disease shows radiolucent changes in the radiograph. Radiolucencies are fuzzy, mottled and blotchy with ragged borders. When the disease becomes chronic, dead bone tissues or sequestra are visible in the radiograph as radiopaque masses surrounded by fuzzy or blotchy radiolucencies.


Treatment for suppurative osteomyelitis involves the use of antibiotics and surgical intervention. The diseased site must be cultured to identify specific pathogens for a definitive antibiotic treatment. Surgical intervention involves debridement, drainage of pus and irrigation of the diseased site. Surgery may also involve resection and removal of sequestrum and the diseased bone with autologous bone replacement.


Baltensperger M, Eyrich G. Osteomyelitis of the Jaws.Springer;2009.

Neville BW, Damm DD, Allen CM, Chi A. Oral and Maxillofacial Pathology. South Asian ed. Elsevier; 2016.

Rajendran R, Sivapathasundaram B. Shafer’s Textbook of Oral Pathology. 7th ed. Elsevier; 2012.

Sapp JP, Eversole LR, Wysocki GP. Contemporary Oral and Maxillofacial Pathology. 2nd ed. Mosby; 2004.

Soames JV, Southam JC. Oral Pathology. 4th ed. Oxford University Press; 2005

Wood NK, Goaz PW. Differential Diagnosis of Oral and Maxillofacial Lesions. 5th  ed. Mosby; 1997.


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