Osteomyelitis and Osteoradionecrosis Flashcards
1
Q
How is Osteomyelitis of jaws classified and what is the origin?
A
- Almost always of local origin and not caused by blood-borne infection
- The classification of osteomyelitis is confusing and not all cases can be easily categorised
- Names are more descriptions of clinical presentations based on chronicity and effects on bone
2
Q
What are the clinical features of acute osteomyelitis and what are the causes?
A
- Bacteria and inflammation spread through medullary bone from a focus of infection
Sources of infection:
-PA infection, pericoronitis, fracture through periodontal pocket, ANUG, contamination injuries (open fractures or gunshot wounds)
Clinical features:
- Mandible mainly affected, usually adult males
- Early complaints: severe, throbbing, deep-seated pain and swelling with external swelling due to inflammatory oedema
- Later: distension of periosteum with pus
- Finally: subperiosteal bone formation causes swelling to become firm. The overlying gingiva and muscle is red, swollen and tender
- Associated teeth become tender and may become loose
- Pus may exude from open socket
- Difficulty opening mouth and swallowing
- Regional lymph nodes enlarged
- Sometimes paraesthesia of lower lip
- Minimal systemic upset
3
Q
What do most pts who suffer from acute osteomyelitis of the jaws have?
A
Jaws are resistant to osteomyelitis, and most pts have a predisposing condition to osteomyelitis
- Local damage or disease of jaws:
Radiation damage
Causes of osteosclerosis which reduces vascularity (Paget’s disease, Fibro-osseus lesions, osteopetrosis)
- Impaired immune defences Poorly controlled diabetes Sickle cell anaemia Chronic alcoholism Drug taking Tobacco smoking Malignant neoplasms and their treatment NB UNCOMMON IN HIV
4
Q
What is the radiographic appearance of acute osteomyelitis
A
- After about 10 days, radiographs show mouth-eaten pattern of bone
- Later shows loss of trabecular patterns and areas of radiolucency indicating bone destruction
- Areas of dead bone appear as relatively dense areas which become more sharply defined as they are progressively separated as sequestra
- Subperiosteal bone formation appears as a thin, curved strip of new bone below the lower border of the jaw in lateral of panoramic radiographs
5
Q
What is the pathology of acute osteomyelitis
A
- Suppurative infection with oral bacteria forming a biofilm on sequestra of bone
- Mandible has relatively limited bone supply and dense bone, so Infection actions and acute inflammation cannot escape => pressure spreading infection though the marrow spaces and compresses BVs confined within their vascular canals
- Thrombosis and obstruction then lead to further bone necrosis
- Pus formed by necrotic soft tissue and inflammatory cells is forced along the medulla and eventually penetrates the cortex to reach the subperiosteal region by resorption of bone
- Distention of periosteum by pus stimulates subperiosteal bone formation, but perforation of the periosteum by pus and the formation of sinuses on the skin or oral mucosa is rarely seen
- At the boundary of healthy and infected tissue, osteoclasts resorb the periphery of dead bone which eventually becomes separated as sequestrum
6
Q
What is the management of acute osteomyelitis
A
- Usually resolves fully following aggressive treatment
- The key factor is to assess whether the infection is limited to the jaws or may be spreading systemically
- Severely ill or very pale pt with high temp suggest systemic spread
- Essentail measures:
Bacterial sampling and culture
Vigorous antibiotic treatment
Debridement and immobilisation of any fracture
Drainage to relieve pressure
Remove source of infection if possible - Additional tx:
Sequestrectomy
Decortication if necessary
Resection and reconstruction
7
Q
What are the clinical features of chronic osteomyelitis
A
- Suppurative infection, but suppuration is generally limited and may cease in quiescent periods
- Much more common than acute osteomyelitis and arises from infection by weakly virulent bacteria or in avascular bone
- Most cases develop without acute phase (rarely acute osteomyelitis develop into chronic - when it does it is usually due to inadequate tx)
Clinical features:
- Mandible mainly affected
- Infection of dental origin
- Low-grade pain (persistent ache or pain, bad taste from pus draining to mouth, may be exposed bone, in more acute phases there is swelling and increased pain)
- Initially the original focus of infection can be identified, but may persist after removal of source of infection and becomes self-perpetuating in the bone
8
Q
What is the radiographic appearance of chronic osteomyelitis
A
- Variable
- Patchy or poorly defined radiolucency and sclerosis (sometimes resembling malignant neoplasm)
- Sequestra may be identified
- There may be periosteal new bone later (proliferative periostitis)
9
Q
What is the pathology of chronic osteomyelitis
A
- Persistent low-grade infection associated with chronic inflammation, activation of osteoclastic bone destruction and granulation tissue formation
- Healing is frustrated by inability of the inflammation immune response to access bacteria in dead avascular bone and by the slow separation of dead bone as sequestra
- Sequestra will usually separate spontaneously during months or years and may be several cm in length
- If antibiotic tx successful, sequestra may be sterilised and reincarnated into healing bone
- Conversely, infection may spread widely but never develop florid features of acute osteomyelitis
10
Q
What is the management of chronic osteomyelitis
A
- Resistent to tx and must be treated aggressively to overcome factors that favour persistence of infection
- Slow response to tx
- Source of infection must be removed
- Prolonged antibiotic tx required
- Role for surgery to remove sequestra, sclerotic and non-vital bone
11
Q
What are the clinical features of diffuse sclerosing osteomyelitis
A
- Even lower intensity of infection, without formation of pus in which low-virulence organisms or repeated inadequate antibiotic treatment may lead to longstanding widespread osteomyelitis
- Persistence of infection not obvious and chronic low-dull pain and swelling are not severe enough to suggest osteomyelitis immediately
Clinical features:
- Affects adults and mandible almost exclusively
- Patchy diffuse sclerosis in alveolar process
- Changes are more marked around sites of PA or periodontal chronic inflammation
- Persistent ache or pain but no swelling
- Some cases may be part of SAPHO syndrome
12
Q
What is the radiographic appearance of diffuse sclerosing osteomyelitis
A
- Main features are radiographic
- Extensively patchy sclerosis of mandible, poorly localised and without a clear focus of radiolucent infection
- Resembles but is distinct from florid cemento-osseus dysplasia
13
Q
What is the pathology and treatment of diffuse sclerosing osteomyelitis
A
Pathology
- Bone sclerosis and remodelling
- Scanty marrow spaces and little or no inflammatory infiltrate, although adjacent to areas of inflammation
Treatment:
- Eliminate source of infection with local measures and antibiotics
14
Q
What are the clinical features of focal sclerosing osteomyelitis
A
- In some cases, a focus of osteomyelitis is so small or caused by such low-virulence organisms that the clinical presentation is dominated by the local bone reaction to the infection rather than the infection itself
- Commoner in young because their bone is better vascularised and produces more reactive bone deposition around the infection
- Suppuration and widespread infiltration of marrow spaces by inflammatory cells are ABSENT
- Bony reaction to low-grade PA infection
Clinical features:
- Children and young adults affected
- Premolar or molar region of mandible affected
- Bone sclerosis associated with non-vital or pulpitic tooth
- Localised by uniform radiodentisty related to tooth with widened PDL space or PA area
- No expansion of jaw
15
Q
What is the pathology and treatment of focal scleroising osteomyelitis
A
Pathology
- Dense sclerotic bone with scanty connective tissue or inflammatory cells
Treatment
- Elimination of source of inflammation by xla or endo
