Osteosclerotic metaphyseal dysplasia, dysosteosclerosis or osteomyelitis? Paediatric case presentation with associated mandibular swelling and a review of the literature

  1. Shima Chundoo 1,
  2. David M McGoldrick 2,
  3. Rhodri Williams 1 , 3 and
  4. Kevin McMillan 1 , 3
  1. 1 Oral and Maxillofacial Surgery, Birmingham Children's Hospital NHS Foundation Trust, Birmingham, UK
  2. 2 Oral and Maxillofacial Surgery, Queen Elizabeth Hospital Birmingham, Birmingham, UK
  3. 3 Oral and Maxillofacial Surgery, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK
  1. Correspondence to Dr Shima Chundoo; shima.chundoo1@nhs.net

Publication history

Accepted:29 Apr 2022
First published:12 May 2022
Online issue publication:12 May 2022

Case reports

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Abstract

Osteosclerotic metaphyseal dysplasia (OMD) is an extremely rare form of osteopetrosis, which bears significant clinical similarities to dysosteosclerosis (DSS). We aim to present a rare case of OMD with mandibular swelling and osteomyelitis infection including diagnosis journey as well as management in 7-year-old patient. Literature review completed for OMD cases. Case report investigative methods include genetic testing, CT facial bones and MRI scan, orthopantogram and bone biopsies. An initial suspected diagnosis of DSS with chronic osteomyelitis was made. However, following genetic testing, a diagnosis of OMD was confirmed. Our patient underwent a surgical debulking procedure and antibiotic treatment. Less than 10 patients with this condition have been reported within the international literature. There is a wide range of presentation. OMD, DSS and osteomyelitis are all within a similar spectrum of bone conditions. Our understanding, regarding OMD, remains limited and, hence, further research is required to elucidate a thorough clinical picture.

Background

Osteosclerotic metaphyseal dysplasia (OMD) is an extremely rare form of osteopetrosis, characterised by osteosclerosis at the metaphyses of long tubular bones.1 2 The skull is seldom affected.1 2 Other features also include developmental delay, hypotonia and late-onset paraplegia.1 2 OMD can often be mistaken for several other bone diseases. It does bear some clinical similarities to dysosteosclerosis (DSS) and hence it can be difficult to establish a definitive diagnosis. DSS was initially described as an extremely rare disorder, characterised by diffuse osteosclerosis with expanded ends of tubular bones and sclerotic platyspondyly.3–6 Other features include short stature, bone fragility, optic atrophy, developmental delay, cranial nerve palsy and failure in tooth eruption as well as noted abnormalities in tooth development.3–6 Presentation is often in early childhood and infancy.3–6 DSS is also sometimes confused with osteopetrosis.3–6 However, there are several key distinguishing features only seen in DSS, including sclerotic platyspondyly, lack of bone marrow dysfunction and no sclerotic changes in diaphyses.3–6

Osteomyelitis is often an underlying feature of several bone conditions, which can make management and treatment challenging. Osteomyelitis is a progressive inflammatory disease.7 It is characterised by bone destruction and sequestrum formation.7 8 The symptoms can often vary and indeed, disease progression can be interluded by periods of quiescence.7 8 The treatment normally involves long-term antibiotics as well as heavy surgical debridement.7 8 The aims of the treatment are to restore function and resolve infection.7 8

There is significant clinical overlap between OMD and DSS. It is imperative that a clear diagnosis is made and often, this requires clinical evaluation and imaging as well as genetic testing to isolate the implicated genes. We present a rare case of OMD in a paediatric patient, and the journey towards developing a definitive diagnosis and treatment plan.

Case presentation

The patient presented at age 7 to our department. He lived at home with his parents and siblings. His medical history included a left inguinal repair, congenital nystagmus and strabismus with a predominant left convergent squint. Previous delayed development was noted historically. There was also positive family history for consanguinity.

Our patient was referred to the unit, a regional Children’s Hospital, from a local dental hospital, due to an ongoing mandibular swelling and exposed lingual bone. On examination, the patient presented with a significant left mandibular swelling and intraoral lingual bone exposure as well as gingival dehiscence. He has been seen regularly on our department since initial presentation. There was a general improvement in his condition for the majority of these reviews, however, on three occasions the patient was admitted for surgical intervention (March 2019, December 2019 and June 2020).

Investigations

A skeletal survey demonstrated diffuse sclerosis, particularly at metaphyses, which also showed alternating radiolucent bands (figure 1). An ‘Erlenmayer flask’ deformity was noted at the proximal humerus. This suggested two possible differential diagnoses, osteopetrosis or dystosteosclerosis.

Figure 1

Skeletal survey.

CT and MRI scans both demonstrated a marked bony abnormality throughout the imaged skeleton with a diffusely increased bone density (figures 2–4). There was a progressive expansion and periosteal reaction involving the left mandible. Consequently, a ‘bone in bone’ appearance was seen. The radiological appearance also showed osteoblastic activity of an unknown aetiology. It was thought that this abnormal bony remodelling was attributed to underlying skeletal dysplasia in response to infection.

Figure 2

CT 3D reconstruction at initial presentation.

Figure 3

Axial MRI scan at initial presentation.

Figure 4

Axial MRI scan at initial presentation.

An orthopantogram radiograph (OPT) reported a sclerotic appearance within the left mandible (figure 5). This was progressively expanding prior to resection. Bone biopsies further revealed light to moderate growth of streptococcus gordonii and staphylococcus aureus which were shown to be sensitive to cefotaxime and penicillin.

Figure 5

OPT at initial presentation. OPT, orthopantogram radiograph.

Haematology and biochemistry investigations at initial presentation were both normal. Finally, our patient underwent genetic testing. This confirmed the patient was positive for a homozygous leucine-rich repeat kinase 1 (LRRK1) gene variant which is implicated within OMD.

Differential diagnosis

Following referral, our patient was seen by the Haematology and Maxillofacial teams as well as undergoing further investigations to determine a definitive diagnosis. A provisional diagnosis of DSS with chronic osteomyelitis affecting the mandible was made. This was corroborated by a CT scan, which showed a diffusely increased bone density. A progressive expansion and periosteal reaction illustrated a ‘bone in bone’ appearance. This was further compounded by an MRI scan, which also noted a ‘bone in bone’ appearance. Oedema within the muscles was also illustrated within the MRI scan. Bony remodelling, seen within the scans, was thought to be associated with skeletal dysplasia in response to a chronic infection.

The additional differential diagnoses, based on the investigations, included osteopetrosis, sclerosing bone dysplasia, fibrous dysplasia as well as low-grade malignancy. However, the patient subsequently underwent genetic testing, which identified a homozygous LRRK1 gene variant, which had been previously associated with OMD. This is autosomal recessive in nature. The patient has a younger sibling who was also subsequently found to demonstrate the same genetic variant.

Treatment

Our patient required three episodes of surgical intervention. Initial intraoral debridement of necrotic bone from the left mandible was completed in March 2019. Unfortunately, there was significant deterioration in the patient’s condition 9 months later. The patient attended clinic with an increase in swelling to the left aspect of the mandible. Clinically there was a fluctuant collection overlying the left mandible and pointing of skin was apparent. This raised a concern for the potential development of an orocutaneous sinus. The patient was admitted for aggressive intravenous antibiotic treatment as well as incision and drainage of the collection under general anaesthetic.

In June 2020, there was a further deterioration in the patient’s condition. He presented with two new extraoral draining sinuses and mild trismus as well as a significant increase in mandibular swelling. CT and MRI scans were completed, which showed vast bony expansion of the mandible, from condyle to symphysis (figures 6 and 7). There was evidence of underlying infection but no collection. Our patient was initially admitted for a debulking procedure, however, on admission; the patient was found to have iron deficient anaemia and significantly low haemoglobin. Consequently, the operation was postponed.

Figure 6

CT 3D reconstruction prior to surgery.

Figure 7

Axial CT slice showing left mandibular bony expansion.

In September 2020, after treatment for his anaemia, the patient was admitted for the debulking procedure of his mandible. This was performed via a transcervical approach and the patient required fixation of a mandibular fracture and multiple lymph node biopsies (figure 8). Post operatively, he developed a left-sided haematoma which was confirmed by ultrasound investigation (figure 9). Blood investigations, completed postoperatively on day 2, revealed a C reactive protein (CRP) level of 251 mg/L and haemoglobin of 48 g/L. Subsequently, our patient underwent a further incision and drainage under general anaesthetic. A unit of red blood cells was also transfused preoperatively. Further blood investigations, completed on day 7, demonstrated a reduction in CRP level to 39 mg/L and corrected haemoglobin of 92 g/L.

Figure 8

Postoperative OPT. OPT, orthopantogram radiograph.

Figure 9

Ultrasound image showing collection in left submandibular region.

Outcome and follow-up

Postoperatively, our patient has been doing well with good oral intake. He reports minimal discomfort. There remain three distinct cutaneous sinuses which are clinically similar to the patient’s preoperative appearance. There is a suggestion of a chronic infective process, which is likely exacerbated by his underlying bone condition. Unfortunately, our patient has been suffering from recurrent headaches. Previous CT scans reported a thickened calvarium, which could potentially led to an increase in intracranial pressure and, therefore contribute to his ongoing headaches. Further neurosurgical input may be required.

Future treatment with regards to an allogenic stem cell transplantation is also due to be considered. Our patient was born to consanguineous parents and has a younger brother, with a similar clinical presentation and associated LRRK1 genetic variant. Genetic counselling and support have been provided to the parents regarding the possibility of future children with similar genetic profiles.

Discussion

OMD is a very rare form of osteopetrosis. Overall, there is a paucity of the literature available on OMD and less than 10 cases have been reported. Previous cases have been characterised by progressive developmental delay, hypotonia, elevated alkaline phosphatase and characteristic radiographic findings of osteosclerosis at the metaphyses of long tubular bones .9–11 The first reported case of OMD, by Nishimura and Kozlowski in 1993, revealed two Japanese siblings of first cousin descent, who reportedly demonstrated a clinical presentation of early developmental delay, hypotonia and late onset paraplegia.9 This was followed in 2003, by Mennel and John, who discussed a 23-month old man demonstrating hypotonia, developmental delay and complex seizures.10 The complex presentation mimicked lead poisoning as the child demonstrated neurological symptoms and sclerotic metaphyseal changes. However, further analysis of the radiographs indicated a diagnosis of OMD. The subsequent case reported a similar picture, including 12-month old man with hypotonia, developmental delay as well as sclerosis of metaphyses.11

DSS was first noted in 1968, by Spranger et al, with a 12-year-old male patient presentation and five similar paediatric presentations.12 This initial report considered additional clinical features, including small stature, increased bone fragility and cranial nerve involvement.12 DSS is a rare form of bone dysplasia, with associated neurodevelopmental features.5 6 DSS has a characteristic radiographic appearance of diffuse osteosclerosis with expanded ends of the tubular bones and platyspondyly. In 1978, a 15-year-old male patient was reported with histological findings, of unresorbed primary spongiosa, consistent with osteopetrosis.13 Subsequent clinical findings demonstrated metaphyseal expansion with osteopenia and cortical thinning, a diagnosis of DSS followed. The patient also presented with short stature, oligodontia, recurrent fractures and cranial nerve compression, leading to blindness and deafness. Further follow-up, by Lemire and Wiebe, revealed the now 44-year-old patient had persistent widening of proximal and distal tubular bones.14 A study by Elcioglu et al also reported three further cases in 2002.5 These cases consisted of two siblings, a 14-year-old woman and 9-month-old man, who were born to non-consanguineous parents. A recently published case, by Whyte et al, in 2010 revealed a 44-month-old woman with frontal bossing, orbital and facial sclerosis and progressive metaphyseal widening.6

A thorough understanding of the genetic process behind disease inheritance and progression would provide an invaluable foundation for targeted treatment avenues. The genetic pathway of DSS remains undetermined. However, as the number of men affected is greater, it has been hypothesised that DSS is either an autosomal recessive or X-linked recessive trait.3–6 Bone marrow transplantation has been suggested as a potential treatment option. However, this treatment modality is ultimately dependent on osteoclast activity and indeed there have been fatal complications associated with bone marrow transplantation. Teriparatide injections have also been hypothesised as a further treatment option.3–6

The genetic basis for OMD, unfortunately, also remains unknown but an autosomal recessive pattern of inheritance has been suggested.1 2 It has been hypothesised that OMD is potentially linked to consanguity.1 2 Studies have also demonstrated that LRRK1 genetic mutations are possibly associated with OMD.1 2 LRRK1 gene consists of 34 exons and encodes 2015 amino acids.1 2 A mutation within this sequence can lead to a defective protein production, which fails to repair the defective LRRK1 osteoclasts.1 2 This, therefore, leads to impaired bone resorption and hypomorphic effect.1 2 However, there is a range of OMD presentations, with and without the LRRK1 mutation.

In 2016, Lida et al reported the first case of OMD, associated with LRRK1 genetic mutations, and a clinical picture of failure to thrive and hypotonia was noted.2 On radiographic examination, the metaphyses showed alternating bands of osteosclerosis and bony undermodelling.2 In contrast, the diaphyses were neither osteopenic nor osteosclerotic. Guo et al further identified a sibling case of OMD, born to non-consanguineous patients, with associated LRRK1 mutations.1 These siblings had normal intelligence and stature but suffered from recurrent fractures. Radiographic examination revealed sclerosis of the metaphyses of long bones. Facial dysmorphism was present in one of the siblings. It was further postulated that sclerotic lesions appear to resolve with age after direct comparison with previous OMD cases associated with LRRK1 mutations.

A recently published case report, in 2015, showed a 12-year-old female OMD patient suffering with interstitial pulmonary lesions and recurrent chest infections.15 This patient also demonstrated hypotonia, developmental delay and hepatosplenomegaly. Interestingly, the pulmonary lesions noted may be a further feature of OMD and requires additional evaluation. In 2020, Howaldt et al reported a 34-year-old patient with osteonecrosis of the jaw associated with an LRRK1 splice site mutation.16 There was no known consanguineous element.16 The case report showed characteristic radiological features, including osteosclerosis of metaphyses and vertebral bodies, as well as short stature and facial dysmorphia.16 This patient was managed conservatively, with debridement of necrotic bone.16 However, a subsequent pathological atraumatic mandibular fracture, with associated soft tissue infection and fistula formation, occurred.16 The patient was, therefore, managed with intermittent bone debridement, surgical drainage and antibiotic treatment.16 Ultimately, there is a wide range of presentation across patient cases.1 10 Crucially, the current literature does not report any mandibular swelling, underlying infection or subsequent management in a paediatric patient.

Radiographic imaging for OMD is characterised by osteosclerosis limited to metaphyses of long tubular bones with osteopenic diaphyses.1 2 These osteosclerotic changes are seen, with reducing severity, in the iliac crest, ends of ribs and clavicles and vertebral end plates.1 2 The baseline imaging of choice for OMD remains skeletal radiographs complemented by clinical examination and genetic testing methods. In our case, the mandibular expansion and superimposed osteomyelitis infection necessitated further imaging methods. Orthopantogram radiographs provided a good image of the entirety of the mandible, associated dentition and an overview of lesion extension.17 However, CT scans are particularly instrumental in determining the size, extent and location of lesions as well as providing further clarification on bone and soft tissue invasion.17 CT scans can equally be used, from a preoperative perspective, to aid in surgical planning.17 18

CT scans can also accurately demonstrate osteomyelitis, which can show medullary sclerosis, periosteal reaction and sequestra formation.17 Equally, MRI scans are valuable in visualising osteomyelitis infections, in particular, bone marrow oedema because of the high soft tissue contrast resolution.17 Nuclear medicine does have some applications in visualising osteomyelitis infections. It can be considered in situations whereby MRI scans are contraindicated.19 Nuclear medicine involves intravenous administration of a radionuclide and permits visualisation of abnormal bone metabolism. In osteomyelitis, there would be an increase in radionuclide uptake. Nuclear medicine imaging techniques demonstrate high sensitivity with full body imaging to assess further sites of infection. However, this imaging modality is limited by poor specificity and anatomical localisation and, therefore, further MRI and CT scans may be necessary to complement the osteomyelitis diagnosis.19 A recent paper by Tiwari et al has suggested that the most sensitive and specific imaging modality for osteomyelitis of the jaw is scintigraphy and single photon emission computed tomography (SPECT) scanning.20

The superimposed osteomyelitis infection, within our case, rendered management difficult. Antibiotics form the basis of treatment for osteomyelitis, including clindamycin and first generation cephalosporins.7 8 21 There are several factors to consider with antibiotic choice, including side effect tolerance, bone absorption and penetration as well as dosage in respect to half life.7 8 21 Investigative tests and measuring treatment outcomes can be demonstrated by blood tests. CRP and C calcitonin levels are useful in measuring patient response. CRP is the most useful indicator due to ease of sample taking and is reportedly more reflective of patient outcomes compared with erythrocyte sedimentation rates.7 8 21

In chronic osteomyelitis, antimicrobials have limited effect and often surgery is the mainstay of treatment.7 8 21 The primary principles of this treatment are to eradicate necrotic bone and leave a viable vascularised bony environment with potential for healing. This heavy debridement leaves a dead space, which often needs reconstruction through skin grafts, muscle or myocutaneous flaps. The use of antibiotic polymethylmethacrylate beads as a temporary filler material has also been suggested.7 8 21 Myocutaneous or free tissue flaps provide reconstruction with both skin and muscle as well as microvascular technique.7 8 21

OMD, DSS and osteomyelitis are all within a similar spectrum of bone conditions, which can prove challenging to treat for physicians and surgeons alike. Indeed, a conclusive diagnosis is instrumental in determining treatment avenues, permitting appropriate prognosis discussions with patients and parents as well as facilitating a deeper understanding into relatively rare bone conditions. The identification of LRRK1 in OMD may also prove to be a target molecule for future drug therapy. The understanding and knowledge with regards to the phenotype associated with OMD and LRRK1 gene mutation remains limited and hence further research and studies are required to elucidate a thorough clinical picture.

Learning points

  • Osteosclerotic metaphyseal dysplasia is an extremely rare form of osteopetrosis and can be easily mistaken for other bone conditions. Osteomyelitis is a complicating feature of several bony conditions, which can make diagnosis difficult.

  • Collaboration with wider medical teams is vital to reach a definitive diagnosis and deliver effective patient care.

  • Genetic testing plays a significant role in determining the diagnosis, patient management and family planning.

  • Genetic counselling, within families, is invaluable in managing a patient and, indeed, a family holistically.

Ethics statements

Patient consent for publication

Footnotes

  • Contributors SC wrote the initial draft of case report. Subsequent review and revisions by DMM, KM and RW.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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